Pulmonary Mechanisms Flashcards
Explain the piston model and how this related to the lungs as a breathing apparatus?
To help identify the forces involved in breathing, consider a simple model of a piston of a certain mass (M), moving down a cylinder. In this model, the piston is attached to the upper cylinder wall by a pair of springs. To move the piston down the cylinder, the applied force must be sufficient to initiate and accelerate the piston down the cylinder at some velocity. In the piston-cylinder model, the three main forces that oppose movement are 1) elastase of the springs, 2) frictional resistance between piston and cylinder wall, and 3) inertia of the piston. These same opposing forces are important in respiratory mechanics as previewed in the table below.
The respiratory muscles must general enough force to? Need what to do this? Where does this come from? How can the force of the respiratory muscles be changed? What are accessory muscles?
The lung resembles a reciprocating bellows pump powered by the respiratory muscles. For breathing, the respiratory muscles must generate sufficient force to overcome the forces that oppose movement of the lung-chest cage. Unlike the sinoatrial node that generates rhythmic contraction of the heart, the respiratory muscles lack inherent rhythmicity. They depend upon motor nerve impulses to initiate contraction and relaxation. The nerve impulses initiating contraction of the respiratory muscles originate in the medullary region of the brain stem. The force generated by the respiratory muscles (rate or strength of contraction) can be increased by increasing the frequency of discharge in individual motor units, activating additional motor units, or by calling upon the accessory muscles of respiration. Accessory muscles refer to muscles not normally used during eupneic (resting) breathing. The respiratory muscles can be divided functionally into two groups: the muscles responsible for inspirationand those involved in expiration.
What are the muscles of inspiration? Expiration?
The muscles of inspiration include the diaphragm, the external intercostals, and the accessory muscles. The diaphragm and external intercostals are the most important muscles of breathing. During inspiration, contraction of the diaphragm and external intercostal muscles enlarges the chest cavity. This action leads to an expansion and stretching of the lung. As the lung inflates, potential energy is stored in the stretched elastic structures of the lung such that with relaxation of inspiratory muscles, expiration occurs from elastic recoil of the lung-chest cage apparatus. Thus, at rest, expiration is normally considered to be passive because muscle contraction is not required.
What is the role of the diaphragm? structure? origin and insertion?
Besides being the principal muscle of inspiration, the diaphragm also separates the thoracic from the abdominal cavity to convert the thorax into a closed chamber. The diaphragm is composed of two muscular hemidiaphragms, joined by a membranous portion at the midline. The origin and insertion of the diaphragm is on the interior surface of the lower ribs and sternum. The center portion of the diaphragmnormally curves upward when relaxed at end-expiration. During contraction, the central portion of the diaphragmbecomes more flattened, similar to a piston moving down a cylinder. In an adult, the diaphragm normally descends about 1.5 cm, with as much as a 10-cm descent during a maximal inspiration. With the downward movement of the diaphragm, the volume of the thoracic cavity and the lungs increase. Normally about two thirds of the tidal volume is directly attributable to diaphragmatic contraction. Motor innervation to the diaphragm originates from the spinal cord at C3 through C5. These nerves join to comprise the phrenic nerve.
Explain the external intercostals? how do they pull? why is this important? their paralysis leads to?
In human, the 12 ribs articulate with the thoracic vertebrae, allowing them to rotate. The external intercostal muscles are attached between adjacent ribs and oriented such that their contraction elevates the anterior end of each rib, pulling it upward towards a horizontal plane. This action increases the antero-posterior diameter of the rib or thoracic cage. From side view, it resembles the action of a “pump handle”. While the importance of external intercostal muscles is overshadowed by the diaphragm, their contraction prevents the rib cage from being pulled downward and inward as the diaphragm descends during inspiration. Intercostal contraction also tenses or strengthens the intercostal spaces so they will not be drawn in by descent of the diaphragm. While the external intercostals can maintain a considerable level of breathing on their own, their paralysis does not prevent ventilation by the diaphragm alone. Innervation of the external intercostals is from the intercostal nerves that arise from the spinal cord at T1 through T12.
Explain the accessory muscles? when are they active? what do they do?
The accessory muscles of inspiration include the scalenes and sternocleidomastoids. These muscles are minimally active during eupnea. Contraction of the scalene muscles elevates the first ribs, whereas the sternocleidomastoids raise the sternum. The accessory muscles are usually inactive until ventilation reaches a fairly high rate of 50 to 100 L/min in an adult. Nevertheless, they are active during ventilation associated with heavy exercise. Additional accessory muscles of the back may also facilitate inspiration at high ventilatory rates.
What are the passive forces of expiration?
During quiet or eupneic breathing, expiration is usually passive. With contraction of the inspiratory muscles to bring about inspiration, elastic components of the lung are stretched. The potential energy stored in the elastic features of the lung is released with relaxation of inspiratory muscles. Elastic recoil of the lung is normally sufficient to bring about expiration without contraction of expiratory muscles. However, with high ventilatory rates, the muscles of expiration comprising the abdominal group and the internal intercostalsare important.
Explain the muscle groups associated with expiration? what are they innervated by? when are they used? The diaphragm does what in the beginning of expiration?
The principal abdominal muscles of the expiratory group include the external and internal oblique and the rectus and transverse abdominus. Contractions of these muscles increase intra-abdominal pressure to force the diaphragm upward. In normal adults, the abdominal muscles may not become active until minute volume is increased several folds from rest (i.e., >40 L/min). The abdominal muscles are innervated by nerve fibers emerging from T-1 through T-12. These muscle groups are inactivated early in anesthesia. However, the abdominal muscles are the principal muscles responsible for coughing and for forced lung expiratory volume measurements, like the vital capacity.
The other muscles of expiration are the internal intercostal. They are attached between adjacent ribs and act antagonistically to the external intercostals. Contraction of the internal intercostals compresses the rib cage to decrease the antero-posterior diameter of the thoracic cage. During coughing their contraction prevents bulging of the intercostal spaces.
The diaphragm is also a participant in expiration. Electrical recordings from the phrenic nerve indicate that the diaphragm continues to contract during the early part of expiration (see bottom figure). Continued diaphragmatic contraction during early expiration opposes some of the lung recoil and results in a slowing of expiration. It also ensures a smooth transition from inspiration to expiration.
explain pulmonary elasticity? elasticity opposes? compliance is what?
The lung is an elastic structure with an anatomical organization that promotes its collapse to essentially zero volume, much like an inflated balloon. The term elastic means a material deformed by a force tends to return to its initial shape or configuration when the force is removed. While the elastic properties of the lung are important to bring about expiration, they also oppose lung inflation. As a result, lung inflation depends upon contraction of the inspiratory muscles. How easily a lung inflates will relate to the compliance of the lung. Compliance is the preferred term to describe the elastic properties of the lung. Compliance is a measure of the ease of deformation (inflation).
explain the relationship of compliance to elasticity?
The lung is an elastic structure with an anatomical organization that promotes its collapse to essentially zero volume, much like an inflated balloon. The term elastic means a material deformed by a force tends to return to its initial shape or configuration when the force is removed. While the elastic properties of the lung are important to bring about expiration, they also oppose lung inflation. As a result, lung inflation depends upon contraction of the inspiratory muscles. How easily a lung inflates will relate to the compliance of the lung. Compliance is the preferred term to describe the elastic properties of the lung. Compliance is a measure of the ease of deformation (inflation).
Compliance = ‘ ‘V/’ ‘P
Low Compliance = Low Distensibility
Low Compliance = High Elastance
HIGH COMPLIANCE = EASY TO INFLATE
LOW COMPLIANCE = HARD TO INFLATE
NEW BALLOON = LOW COMPLIANCE = HARD TO INFLATE
OLD BALLOON = HIGH COMPLIANCE = EASY TO INFLATE
OLD LUNG = HIGH COMPLIANCE = EASY TO INFLATE
YOUNG LUNG = LOW COMPLIANCE= HARD TO INFLATE
EMPHYSEMA = HIGH COMPLIANCE = EASY TO INFLATE
PULMONARY FIBROSIS = LOW COMPLIANCE = HARD TO INFLATE
Explain the lung compliance curve?
If the lung is removed from the thoracic cage, it closely resembles a collapsed balloon. When pressure inside the lung equals outside pressure, or transmural pressure is 0, lung volume is close to zero. Compliance of the lung can be obtained by plotting lung relaxation or recoil pressure (x axis) as a function of lung volume (y axis). Starting from essentially zero lung volume, a measured volume of air is put into the lung and the recoil or relaxation pressure associated with the addition of that air volume is recorded. When repeated in several steps by the sequential addition of measured air volumes and recording of the corresponding recoil or relaxation pressures, a compliance curve for the lung can be constructed. The slope of this plot is lung compliance. Normally, lung compliance is measured under static conditions, meaning no airflow is present at the time the relaxation (recoil) pressure is measured.
Explain the chest compliance curve?
The chest cage also demonstrates compliance characteristics. However, the structure of the chest cage is quite different from the lung. The chest cage would be more analogous to a punctured tennis ball than a balloon. The bony, moderately inflexible rib cage dictates that the chest cavity has considerable air volume when inside and outside pressure are equal, or transmural pressure is 0. Starting at this initial or equilibrium volume of the thoracic cage, in the absence of the lung, it is theoretically possible, though totally impractical, to construct a compliance curve for the chest cage by the incremental addition or removal of measured air volumes. With the sequential addition of air to the chest cavity from its equilibrium volume, a positive (above atmospheric pressure) recoil pressure would result with each air volume addition. On the contrary, if the chest cage is returned to its equilibrium volume and a measured volume of air is removed, a “negative” (below atmospheric pressure) recoil or relaxation pressure would result. A “negative” recoil pressure reflects the tendency of the chest cage to re-expand or return to its equilibrium volume, which would be a larger volume. As more air is incrementally removed from the chest cage, the bony structure of the rib cage soon limits further chest cage compression. At this point, volume changes become minimal, but recoil pressures become increasingly “negative”, as indicated on the left side of the chest wall relaxation curve. As shown, both positive and “negative” recoil or relaxation pressures are plotted on the x axis.
The combined lung and chest compliance curves give?
The relaxation curve:
With the lungs placed insidethe chest cavity and their respective pleural surfaces held together by cohesive forces, the volume of the lung is higher than its equilibrium volume, whereas chest cavity volume is less than it’s equilibrium volume. Thus, the equilibrium volume of combined lung-chest cage represents a point where the tendency of the lung to deflate (to zero volume) is balanced by the tendency of the chest cage to expand. In other words, at the equilibrium volume of the combined lung-chest cage, the lung is expanded above and the chest cage is compressed below their respective equilibrium volumes. The equilibrium volume of the combined lung chest cage corresponds to resting end expiration, or the position (volume) the combined lungchest cage would assume when the respiratory muscles are relaxed. At resting end expiration, the recoil pressure of the lung tending to deflate is opposed to an equal but opposite recoil pressure of the chest wall tending to expand. These equal but opposite recoil forces are reflected by an intrapleural pressure that is typically below atmospheric pressure. Moreover, as a person inhales to expand the chest cage and lung, intrapleural pressure becomes increasingly subatmospheric, reflecting the force tending to separate the lung and chest wall, but this is prevented by the cohesive forces.
What are several important features about the relaxation curve?
The figure below shows separate relaxation curves for the lung (right) and the chest cage (left), along with the combined lung-chest cage relaxation curve (middle). Note that the combined lung-chest cage curve is the algebraic sum of the separate lung and chest cage curves. The slope of each relaxation curve corresponds to the compliance for the structure(s). At end expiration (point A), recoil or relaxation pressure for the lung (right) and chest cage (left) alone are equal but opposite. At this point, lung volume corresponds to functional residual capacity (FRC). As additional air volume is inhaled into the lung, the lung is stretched further and exhibits a greater recoil pressure. At the same time, the chest cage is less compressed, so its negative recoil pressure diminishes as it approaches its equilibrium volume. When a slightly larger air volume is inhaled, the chest cage reaches its equilibrium volume (0 relaxation pressure; point B) and the lung and lung-chest relaxation curves intersect (point C). Thereby, at this lung volume, all measured relaxation for the lungchest cage system is from the lung because the chest cage is at its equilibrium volume (point B), or the volume it would assume if the lung were not present. If an even greater air volume is inhaled (point D), both the lung and chest cage are stretched beyond their equilibrium volumes. Note that the compliance curve for the combined lung-chest cage becomes more flattened (less compliant) at this point because the lung and chest cage are both tending to recoil towards smaller equilibrium volumes. If the total lung-chest cage system is returned to resting end expiration (point A) and air is expelled, a negative relaxation pressure results for both the chest cage and the combined lung-chest cage (point E). At this point, the chest cage is compressed as more and more air is expelled, with the negative recoil pressure reflecting its tendency to expand towards its equilibrium volume (point B). At the same time, the lung contributes little positive relaxation pressure because it is close to its equilibrium volume (i.e., 0 volume) because it is stretched very little.
how do we compute total pulmonary compliance?
During eupneic breathing, the normal tidal volume range is between points A and B. During inspiration, the individual moves up the lung-chest cage compliance curve from Point A towards Point C and in the opposite direction during expiration. Note that over the normal tidal volume range, total pulmonary compliance (combined lung-chest cage) is less than the compliance of either the lung or chest cage alone. This occurs because the lung and chest cage are physically arranged in a serieswith one another. Compliances arranged in series are added as reciprocals to compute total compliance (lung-chest cage compliance), as shown in the equation below the figure.
How do we measure lung compliance in people?
Many pulmonary disorders can alter compliance of the lung, chest cage, or both. Thus, a measurement of compliance can be a useful clinical assessment of a patient’s respiratory system. To determine compliance of the respiratory system, changes in transmural pressures (Pin-Pout) immediately across the lung or chest cage (or both) are measured simultaneously with changes in lung or thoracic cavity volume. Changes in lung or thoracic cage volume are determined using a spirometer with transmural pressures measured by pressure transducers. For the lung alone, transmural pressure is calculated as the difference between alveolar (PA; inside) and intrapleural pressure (Ppl; outside). To calculate chest cage compliance, transmural pressure is Ppl (inside) minus atmospheric pressure (PB; outside). For the combined lung-chest cage, transmural pressure or transpulmonary pressure is computed as PA-PB. PA pressure is determined by having the subject deeply inhale a measured volume of air from a spirometer. The subject then exhales measured air volumes in several steps. After each expired air volume, the subject seals his or her mouth around a manometer and completely relaxes the respiratory muscles with the glottis open. The pressure recorded at the mouth is called relaxation or recoil pressure because the respiratory muscles are relaxed. In addition, the pressure measured at the mouth is the same as alveolar pressure (PA) because the airway is open to the alveoli and no air flow is present (static conditions). Intrapleural pressure is approximated by convincing the subject to swallow a balloon, attached to a pressure transducer, into the esophagus. Esophageal pressure closely reflects average intrapleural or intrathoracic pressure. Thus, compliance curves can be constructed for the lung, chest wall, and total pulmonary system, using the equations presented in the figure.
what are the equations for compliance in people?
What are some factors that affect chest wall compliance?
Chest wall compliance varies from one individual to another, depending on the diameter and shape of the chest and height of the individual. People with deformed chest or musculoskeletal disorders such as kyphoscoliosis often exhibit decreased rib cage mobility, which is manifested as a decrease in chest cage compliance. Likewise, obese people often have reduced chest cage compliance because abdominal fat impedes normal descent of the diaphragm and upward movement of the rib cage during inspiration. While body position does not alter chest wall compliance per se, it may result in a shift in the chest cage compliance curve due to the effect of gravity. This is likely to be encountered as one goes from the upright to the supine position.
What are some factors contributing to lung elasticity?
The lung is an organ that exhibits elastic characteristics. It is one of the few organs of the body whose size can and does change dramatically. When the lung is inflated by contraction of the inspiratory muscles, it is stretched and recoils back to the pre-stretched position upon relaxation of the inspiratory muscles. It is important to consider the factors that impart elasticity to the lung because several clinical disorders, such as pulmonary fibrosis and emphysema, are known to alter the elastic properties of the lung.
Explain surface tension in a sphere? (LaPlace)
The fluid film lining alveoli assumes a spherical shape because of the nearly spherical nature of alveoli. In many regards, the fluid film lining alveoli resembles a soap bubble. In a soap bubble, the relationship between pressure and surface tension is related in an equation derived by LaPlace for spherical objects. The LaPlace equation states that the distending (inflating) or collapsing (recoil) pressure for a soap bubble is directly related to surface tension of the air-fluid interface and inversely related to the radius of the sphere.
explain how to use the law of laplace to see alveolar instability?
If alveolar surface tension is assumed to be constant, say 50 dynes/cm, then the recoil (collapsing pressure) could be calculated for alveoli of different radii using the LaPlace equation (see top figure). Using arbitrary units for radius and pressure, the calculations indicate that alveolus A, with a radius of 1 unit, has a higher pressure than alveolus B, with a radius of 2 units. Since all lung alveoli are interconnected by the airways, the higher pressure in alveolus A would cause it to discharge its air volume into alveolus B. According to the LaPlace equation, as the radius of alveolus A becomes progressively smaller as air moves to alveolus B, pressure in alveolus A steadily increases as the radius decreases with deflation. At the same time, pressure in alveolus B declines further because its radius increases as it fills with air. The implications for the lung as a whole are that alveoli with smaller radii (high pressure) would empty their air volume into larger alveoli and eventually collapse. In a short time, most of the air in the lung would be contained in a few large-radius alveoli, with most remaining alveoli collapsed. Such alveoli instability would result in a marked reduction in surface area for gas exchange.
Explain alveolar opening pressure mathematically?
Alveolar instability would not only result in smaller radii alveoli dumping their air into larger alveoli, but collapsed alveoli, or those with extremely small radii, would require extremely high opening pressures to inflate. Thus, freshly inspired air would be directed towards large-radii alveoli (alveolus B) because the pressure required to expand them would be less than that to inflate collapsed or small-radii alveoli (alveolus A). In fact, if alveoli had a constant surface tension, it is unlikely that the respiratory muscles would be able to generate sufficient pressure (force) to inflate smaller radii alveoli because of their high opening pressures. Likewise, if ventilated alveoli collapsed during expiration, it would be difficult to inflate them on the next breath because of the high opening pressures associate with their small radius (figure).
Explain the physiochemical properties of surfactant?
The ability of surfactants to lower surface tension is related to their chemical structure. Because lung surfactants have hydrophobic (water-fearing) and hydrophilic (water-loving) groups at different ends of the molecule, they preferentially accumulate at the liquid-air interface. At the interface, the hydrophilic end of the molecule extends into the liquid and the hydrophobic end projects into the air phase above (see top figure). Surfactant naturally accumulates at the liquid-air interface to reduce the number of water molecules that would normally occupy the interface. The presence of surfactant molecules disrupts attracting forces between water molecules to reduce surface tension. Moreover, as surface area is decreased, such as when an alveolus deflates, the relative concentration of surfactant molecules per unit area tends to increase. This higher concentration of surfactant molecules is even more effective in reducing surface tension (see bottom figure). As alveoli inflate, water molecules must be brought to the interface, so surface tension increases as fewer surfactant molecules are present per unit area. The LaPlace relationship is still applicable, however, alveolar surface tension is not constant but decreases as alveolar radius decreases. As a result, pressures in small-radii alveoli are less than in large-radii alveoli. During inspiration, air initially moves into smaller radii alveoli or from larger to smaller alveoli to ensure uniform filling of all alveoli. Also, the presence of surfactant reduces the opening and expanding pressures of small-radii alveoli. This enhances alveolar stability and reduces the work of breathing. Surface area matters.
What are the functions of lung surfactant?
Because pulmonary surfactant lowers surface tension as alveolar radius decreases, alveolar pressure (PA) is typically lower in smaller than in larger-radii alveoli during lung inflation. This causes smaller -radii alveoli to fill with air before the larger-radii alveoli because opening or expanding pressures are lower. In addition, atelectasis (alveolar collapse) is prevented at end expiration because surface tension is low in alveoli with small radii. Surfactant also promotes alveolar stability along with alveolar interdependence. Surfactants also aid in keeping alveoli “dry” because if alveoli had a high surface tension, it would tend to draw fluid into the alveoli. Overall, the presence of surfactant lowers the muscle work necessary to inflate the lung. At the same time, surface tension increases as alveoli inflate, which contributes to lung recoil.
Explain the work of breathing?
WORK OF BREATHING: Most of the work of normal breathing is done during inspiration to overcome elastic recoil of the lungs. In addition, during inspiration work must be done to overcome frictional resistance in airways, as well as a very small amount of viscous resistance in rearranging lung tissue as the lungs inflate. During expiration, the relatively small amount of resistance of airways and tissues is more than taken care of by the natural elastic recoil of the lungs: thus, quiet expiration is essentially a passive process not requiring any additional work input by the respiratory muscles.
Explain Ohm’s Law applied to frictional resistance to airflow?
The hydraulic equivalent of Ohm’s law states that resistance to airflow is computed by dividing the pressure difference between two points in the airway or driving pressure by the airflow rate. To compute total airway resistance in man, the pressure difference between the mouth and alveoli should be measured at a given flow. While it is difficult to measure alveolar pressure directly, a subject can be placed in a whole body plethysmograph. The plethysmograph allows alveolar pressure to be measured indirectly, so airway resistance can be estimated using Ohm’s equation.
Explain Pousilles law related to frictional resistance to airflow?
Poiseuille’s law was derived to calculate airflow resistance through a tube, such as an airway. Unlike Ohm’s law, which considers pressure and flow, Poiseuille’s law takes into account the physical dimensions of the tube (radius and length) and the nature of the fluid moving through the tube. Poiseuille’s equation states that frictional resistance to flow is directly related to viscosity of the fluid and length of the tube and indirectly related to the fourth power of tube radius (r4). It is apparent from this equation that if tube radius is halved, without altering tube length or fluid viscosity, the calculated resistance would increase 16-fold. Or, if tube radius is halved, the driving pressure would need to increase 16-fold to maintain the same flow. Poiseuille’s equation was derived using rigid, perfectly round and smooth, nonbranching tubes with an organized or laminar flow pattern. However, lung airways are distensible, compressible, and not perfectly round or smooth. Furthermore, lung airways branch repeatedly and exhibit changes in radius and length during each breath. Poiseuille’s equation also does not compensate for changes in the airflow pattern such as from laminar to turbulent, where frictional resistance is higher.
laminar vs. turbulent airflow?
Laminar or streamlined flow is characterized by concentric cylinders of air flowing at slightly different velocities. Air closest to the wall of the cylinder has the lowest linear velocity (flow rate) and flow velocity gradually increases towards the center of the airway lumen. When viewed in profile, laminar flow exhibits a parabolic pattern. In contrast, turbulent air flow is more chaotic and disorganized.
Explain reynolds number
The transition from laminar to turbulent flow is predicted by Reynold’s number. Reynold’s number is a dimensionless number obtained by multiplying the density of the fluid by the linear velocity of flow and tube diameter, which is all divided by the viscosity of the fluid. If Reynold’s number exceeds an arbitrary value of 2000, it is highly probable that a turbulent flow pattern is present. The presence of turbulent flow requires a greater driving pressure to generate a given airflow than is necessary with laminar flow. Or, frictional resistance to airflow is greater with a turbulent than laminar flow pattern.
Explain the distribution of airway resistance?
About 40% to 50% of the total airway resistance is located between the nose and larynx (see top figure). The remaining resistance resides between the larynx and alveolar ducts (intrathoracic airways). Total airway resistance is slightly higher with nasal than with open-mouth breathing. However, it is within the tracheobronchial tree that several lung disorders are most likely to alter airway resistance. Within the tracheobronchial tree, most resistance to airflow occurs in the medium-sized bronchi between the fourth-to-eighth order of branching. These midsized bronchi offer more air flow resistance than larger or smaller airways because of the complex relationship between air flow velocity, total cross-sectional area, airway length and diameter, and branching frequency. Even though airways become narrowerafter each branching, which would be expected to increase flow resistance, the flow is divided into two parallel paths, so flow velocity in individual airways decreases. A lower flow velocity diminishes the likelihood of turbulent flow. Also, resistances arranged in parallel are added as reciprocals of their individual resistances. As a result, airways distal to the mediumsized bronchi account for progressively less of the total airway resistance. Increased airway resistance offered by the bronchioles and smaller airways is often difficult to detect because they represent such a small fraction of total airway resistance. As a result, these distal airways are sometimes referred to as the “silent airways” because they can have a marked increase in resistance without appreciably altering total airway resistance. However, some pulmonary function tests are capable of detecting increased resistance in the distal airways.
explain airway resistance in the tracheobronchial tree in regards to linear flow of velocity and cross sectional area. and resistance in regards to airway branching number
explain radial traction and transmural pressure?
What are physiological factors that affect airway resistance?
The autonomic nervous system innervates the smooth muscle and secretory glands that surround the airway lumen from the trachea to the alveolar ducts. Parasympathetic cholinergic fibers (acetylcholine as transmitter) of the vagus nerve trunk stimulate constriction of airway smooth muscle and increase secretion of glandular mucus. Thus, increased parasympathetic stimulation tends to narrow the airway lumen from greater muscle contraction and mucus secretion to increase airway resistance.
Sympathetic adrenergic fibers, especially those mediated via beta2 adrenergic receptors, cause smooth muscle relaxation and inhibit mucus gland secretion. Thus, sympathetic stimulation tends to reduce airway resistance. Various chemical irritants, like smoke and dust, stimulation of arterial chemoreceptors, or release of histamine and certain prostaglandins, can also evoke airway constriction. In addition, a local decrease in airway CO2 may cause bronchoconstriction, while an increase in airway CO2 can evoke bronchodilation.
Maximum expiratory flow?
Cartilage and mechanical tethering from neighboring air-ways oppose the tendency of conducting airways to collapse during expiration. Because this tethering increases as lung volume increases, the airways resist collapse when lung volume is high. At low lung volumes flow becomes effort independent because the reduced mechanical tethering cannot oppose the tendency towards air-way collapse that always occur during expiration. Moreover, at progressively lower and lower lung volumes, the flow becomes effort independent earlier. When a person expires with great force, the expiratory air flow reaches a maximum flow beyond which the flow cannot be increased even with greatly increased additional effort. This is the maximum expiratory flow. However, the maximum expiratory flow is much greater when the lungs are filled with a large volume of air than when the lungs are almost empty. Increased effort forces air from the alveoli into the bronchioles, however, the increased effort also tends to collapse the bronchioles. The collapse of the bronchioles greatly increases the airway resistance and opposes the movement of air. That is, the expiratory force is opposed by increased resistance. Once the bronchioles have become almost completely collapsed, further expiratory effort can still increase alveolar pressure, but it also increases the airway resistance by an equal amount, thus preventing any further increase in flow. Therefore, beyond a critical degree of expiratory force, the maximum expiratory flow has been reached. Note that as the lung volume becomes smaller this maximum expiratory flow also becomes less. This is because in the enlarged lung the bronchi and bronchioles are held open partially via elastic pull on their outsides by lung structural elements.
