Ventilation Patterns
Breathing consists of the cyclic action of the lungs to inspire and expire atmospheric gases. Inspiration occurs when the diaphragm and intercostal muscles contract, generating a negative pressure in the pleura surrounding
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TABLE 5.6 Effect of Dead Space Volume, Tidal Volume, and Breathing Frequency on Alveolar Ventilation at a Fixed Minute Ventilation (Vj = 58.0 L/min). Modified from Chemiack.26
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Vn, alveolar gas volume; VD, dead space volume; Vp tidal volume; f, breathing frequency |
Air entering alveolar spaces but not partaking in gas exchange due to poor perfusion of individual alveoli is not part of VA but adds to the total dead space volume (VD). This additional dead space leads to the concept of a physiological dead space that includes not only an anatomical component
(conducting airways) but also a functional component (poorly perfused or
Nonperfused alveoli). Diseases affecting either conducting airway geometry or pulmonary perfusion can thus alter VD. The total volume of air ( -500 mL) inspired (or expired) during each breath is known as the tidal volume. VT and can be described by
VT = VD + ^ , (5.34)
Where f = breathing frequency (breaths min ) so that
VW(Vr-VD). (5.35)
Expired minute ventilation, VE, defines the gas volume inspired or expired in 1 minute and is given by
= Vrf i (5.36)
Typical VЈ for normal quiet breathing is approximately 6-8 L/min. In extreme circumstances, individuals can live for brief periods with minute ventilation rates as low as 1-2 L/min or as high as 300 L/min. Table 5.6 shows the dependence of on VD, VT, and f for a given VE.
Alveolar ventilation supplies 02 to the bloodstream while alveolar capillary perfusion provides alveolar gas with C02. Resting individuals consume
Approximately 250 mL 02/min and produce approximately 200 mL C02/min because, stoichiometrically, metabolic processes require a greater supply of 02 than the quantity of C02 produced. Defining the respiratory exchange ratio, R, as
R = (5.37)
Then R = 0.8 during normal resting breathing andVA = 4 L/min is required to lower the arterial C02 partial pressure to 40 torr and raise arterial 02 partial
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Ments. The curve represents both tidal and forced breathing patterns. |
Pressure to 100 torr in order to maintain blood hemoglobin saturation levels (97.5%) in the venous end of pulmonary capillaries. A corresponding pulmonary perfusion rate, Q, equal to 5 L/min of arterial blood is necessary when both ventilation and flow are uniform. The subsequent ventilation-perfusion ratio, VA/Q, provides a quantitative measure of gas exchange efficiency. Va/Q== 0.8 in this ideal case but generally ranges from 1.0 at rest to 5.0 or greater during heavy exercise.
Summing the inspiratory reserve volume (IRV), the expiratory reserve capacity (ERV), and the residual volume (RV) gives the total lung capacity (TLC). IRV is the maximum additional volume one can inspire from end-tidal inspiration. ERV measures the maximum additional volume one can expire from an end-tidal expiration level. RV measures the gas remaining in the respiratory tract after the maximum possible exhalation and reflects the minimum noncollapsible volume (under normal circumstances) within the airway. In contrast, the functional residual capacity (FRC) measures the gas volume remaining in the airway at an end-tidal exhalation. The deepest possible breath (TLC-RV) is defined as the vital capacity (VC). Figure 5.20 graphically depicts the various components of airway volume. Values for TLC, VC, and RV depend on health, body size, gender, and age. Tabie 5.7 lists predictive equations for healthy individuals. In general, females have 10-25% smaller volumes than men of the same age and size. Age has its greatest effect on RV, which increases by 50% or more from age 20 to age 60.
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TABLE 5.7 Predictive Equations for Static Lung Volumes and Dynamic Pulmonary Function26
A = age (years); H = height (cm); W = weight (kg) “’Health Survey for England (1996) Http://www. official-documents. co. uk/document/doh/survey 96/ehch3.htm#.3.7 |
Forced expiration is commonly used to assess pulmonary function in both healthy and impaired individuals. Static measures of lung volumes (TLC, VT, FRC) fail to detect dynamic changes in pulmonary function that are attributable to disease (e. g., asthmatic airway constriction). Obtaining maximum expiratory flow-volume (MEFV) curves (Fig. 5.21) permits derivation of key parameters in detecting changes in lung function.
Forced vital capacity (FVC) quantifies the maximum air volume expired following a maximal inspiration and is one of the basic measures of analyzing flow changes such as reduced airway patency observed in asthma. To measure FVC, an individual inhales maximally and then exhales as rapidly and completely as possible. FVC primarily reflects the elastic properties of the respiratory tract. The gas volume forcibly expired within a given time interval, FEV, (where t is typically one second, FEV; 0)
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FEV, o = 3.5 L |
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0 |
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FEV1-0/FVC = 87.5% |
FVC
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Is also commonly used for diagnostic purposes and represents expiratory flow resistive properties of the respiratory tract. FEVj 0 has the advantage of being relatively independent of effort and sufficiently sensitive to detect airway obstruction even at low flows. Other timed expiratory intervals are either too short (FEV0 5) and dependent on effort, or too long (FEV2.o) and include low flows occurring at the end of expiration. The FEVj q/FVC ratio quantifies the percentage of FVC expired in one second and is often used to detect changes in flow resistance (e. g., asthma) or airway restriction (e. g., pulmonary fibrosis, obesity). Another common measure of lung function derived from the MEFV curve is the peak expiratory flow, PEF, which is used as a simple method to predict airway conductance. Unfortunately, PEF is sensitive to effort during testing, depends much more on extratho — racic and tracheal conductance rather than pulmonary conductance, and is insensitive to lesser airway obstruction.
5.2.3.2 Intra-airway Airflow Patterns
Transporting inspired and expired gases through the airway, depositing particulates onto mucosal surfaces, and exchanging heat and water vapor between the airstream and airway surfaces depends on a number of factors, one of the more important being airway flow characteristics. Airway geometry, airstream velocity, and gas density determine the flow regime prevailing in each airway region. Turbulence in fluid flow through a conduit is generally associated with fluid inertial forces greatly exceeding fluid viscous forces
Such that Poiseuille flow (parabolic laminar flow) is not established and eddy currents develop. The Reynolds number, Re, quantifies this relationship between inertial and viscous forces and is given by
P
Where /a = fluid viscosity, D = tube diameter, u = mean fluid velocity, and p = fluid density. The equivalent diameter, De = 4A/P, where A = conduit cross-sectional area and P = wetted perimeter, replaces D for noncircular conduits. In circular straight tubes, Re > 2300 typically indicates the presence of turbulence. Convection caused by eddy currents enhances deposition of buoyant airborne particles by bringing more of these particles into contact with the mucosal surface. Airway heat and water vapor exchange is also enhanced by turbulent airflow.
Turbulence in nasal cavity airflow is a consequence of both high airstream velocities, caused by small nasal cross-sectional areas, and very irregular nasal airway geometry, which induces flow distortions. Nasal turbinate Re exceeds 2300 even during normal quiet breathing and nasal cavity airflow is apparently turbulent at most VE. Flow in the pharynx, larynx, and trachea is also generally turbulent at most VE despite Re > 2300 only at higher VE (30 L/min and greater). This airstream mixing enhances convective heat and mass transfer in extrathoracic airways and plays a major role in airway defense mechanisms.
Humans preferentially breathe nasally, possibly because of the highly efficient filtration, humidification, and warming performed on the inspiratory airstream, but inspiratory flow passing through the convoluted passageways incurs a substantial pressure drop. Filtration by the oral cavity is much less effective, but the pressure drop is also lower. As a result, humans normally breathe nasally until VE reaches approximately 30 L/min, when oronasal breathing begins. This shift in breathing pattern occurs because, at lower flow rates, the pressure gradient between the atmosphere and pulmonary airways generated by inspiratory negative pressure in the lungs can overcome nasal resistance, but as flow rates increase, the nasal cavity pressure drop increases proportionally with Re. Consequently, oral breathing must supplement nasal breathing above roughly 30 L/min in order to maintain respiratory airflow. Since flow through the oral cavity has a lower pressure drop than flow through the nasal cavity, a greater proportion of airflow during oronasal breathing passes through the oral cavity. It is unclear whether oronasal breathing produces laminar or turbulent airflow in the oral cavity, though Re < 2100 at VЈ =Ј 30 L/min.
Pharyngeal turbulence results from the 90° bend at the nasopharynx and irregular surfaces at the oropharynx and larynx. Vocal cords constrict the passageway and cause significant flow distortions and turbulence within the larynx. The passageway abruptly expands from the laryngeal orifice into the trachea. Rapid expansion produces a jet in proximal tracheal airflow and turbulence all along the trachea. Turbulent tracheal airflow occurs because the abrupt expansion causes reverse flow in the boundary layer, causing flow separation in the proximal trachea (Fig. 5.22). Under these conditions, turbulence forms at Re much less than 2300 in an abrupt expansion (often at Re = 300).
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FIGURE 5.22 Schematic depiction of airflow pattern through the larynx. Note how eddies form downstream as air passes through the tracheal jet created by the vocal cords. This effect varies according to vocal chord position. |
Studies of airflow through models of bifurcating airways27’28 show that turbulence generated in the trachea does not sufficiently decay in the largest bronchi to produce laminar flow. Despite Re diminishing to below 1000, flow through at least the fourth generation bronchi is believed to be turbulent at all but the lowest Vf. Eventually, however, flow disturbances dampen along the bronchial tree and flow becomes laminar. Entrance flow predominates because bronchi are typically only three to four diameters long. In addition, bifurcations modify velocity profiles because of asymmetric shear forces along inner and outer walls possibly caused by flow separation along the outer wall near the bifurcation (Fig. 5.23). Consequently, disturbed laminar flow appears to exist during both inspiration and exhalation in most bronchi.
Mean airstream velocity diminishes as inspiratory flow moves toward the lung parenchyma because of the rapid increase in total cross-sectional area. The largest increases in area occur in the distal bronchioles and pulmonary airways, causing u to approach zero because
« = j, (5.39)
Where Q = volumetric flow rate (VЈ). Although flow is laminar, Poiseuille flow does not occur despite Re < 1.0 because of the complex geometry of these airways. Axial diffusion (also known as Taylor dispersion) accounts for mass transport within distal bronchioles and combines convection and diffusion in an oscillating fluid with a low Re such that
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FIGURE S.23 Airstream velocity profiles through a bronchial bifurcation. Shear forces along the medial bronchial wall cause flow distortions in the daughter tubes during inspiration. Bimodal velocity profiles generated in the parent tube during expiration are also caused by shear along the daughter tube medial walls. Modified from Scherer and Haselton.28 |
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(5.41) |
Where c = solute concentration; ;e = direction of airflow; y, z~ transverse directions to flow; and K = dispersion constant. K depends on the molecular diffusion coefficient, Dal), where Fick’s law defines mass transport by molecular diffusion as
~D*hAdx ’
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K = f |
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(5.42) |
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( ^ab> Jj |
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Where U = convective velocity. Pulmonary airways rely solely on molecular diffusion for mass transport. Mucus gel floating on airway periciliary fluid becomes contaminated by atmospheric contaminants deposited onto the air-mucus interface during respiration. Deposition generally traps these materials, especially particulates, in the mucus gel and prevents them from being transported further by the airstream. Merely trapping these materials, however, serves little purpose because they would diffuse through the periciliary fluid to enter the epithelia and blood- |
So that
stream. Cilia projecting from the apical surface of ciliated columnar epithelial cells, however, continuously propel mucus toward the epiglottis. Given sufficient mucus velocity, trapped contaminants will reach the epiglottis before they can diffuse through the periciliary fluid in sufficient quantity to cause injury or disease. Swallowing passes the contaminated mucus into the esophagus and eliminates the threat to the respiratory tract.
Cilia are present along most extrathoracic airway surfaces except for the nasal vestibule, olfactory surfaces, nasopharynx, oropharynx, oral cavity, and portions of the larynx. Extrathoracic airway cilia gradually push mucus distally toward the epiglottis. In nonciliated regions, mucus moves by mechanical force (coughing, sneezing, and swallowing) or by gravity. Cilia line all tracheobronchial surfaces down to the pulmonary airways, propelling mucus proximally toward the epiglottis. Respiratory airway surfaces (respiratory bronchi, alveoli) are devoid of cilia.
Ciliary Structure
Cilia are thin cylindrical hair-like structures with a cross-sectional radius of 0.1 (Jim projecting from the apical epithelial surface of ciliated columnar cells. Ciliary length is thought to correspond to periciliary fluid depth and range from approximately 7 |xm in proximal airways to roughly 5 |xm in more distal airways.-9 Each ciliated epithelial cell supports approximately 200 cilia at a density of eight cilia/p, m2. Short microvilli, possibly associated with secretory functions, are interspersed among the cilia.
Nonciliated cells separate fields of ciliated epithelial cells from each other. Synchronized ciliary movement, with a beat frequency in human proximal airways under normal conditions of 8—15 Hz,30-34 propels mucus along the mucociliary escalator at a rate of up to 25 mm/min.35,36 Beat frequencies appear to slow to roughly 7 Hz in more distal airways. Cilia move in the same direction and in phase within each field but cilia in adjacent fields move in slightly different directions and are phase shifted. These beat patterns result in metachronal waves that steadily move mucus at higher velocities ( = 12-18 mm/min) than would be achievable by summing the motion of individual cilia.
Relationship of Ciliary Motion to Mucus Movement
Mucus gel is propelled toward the epiglottis by a two-phase ciliary bear cycle. Forward mucus movement occurs during the effective or power phase of the cycle, when cilia fully extend and traverse an arc perpendicular to the epithelial surface (Fig. 5.24). Claw-like structures, 25-35 nm long, project from each cilia tip and appear to assist in the mechanical transfer of momentum from cilia to mucus gel. Maximum mucus velocity depends on the extent cilia penetrate the epiphase during the power phase, periciliary and mucus gel viscosity, and cilia density.
During the recovery or preparatory phase, cilia bend over, swing back to start position generally parallel to the epithelial surface, and stiffen in anticipation of the next power phase. Ciliary bending and axial movement
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Power stroke |
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III
Net mucus movement FIGURE 5.24 Components of ciliary movement, (a) Power and recovery phases of ciliary movement. Arrows indicate the direction of ciliary travel, (b) Net mucociliary transport. Dotted arrows show the direction of cilia while the solid arrows show mucus transport. Note that net gel movement is forward in I and III while no gel movement occurs in II during the cilia recovery phase. Modified from Ful — ford and Blake.29 |
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Recovery period |
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X |
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Ui) X |
Parallel to the cell surface significantly reduce retrograde momentum exerted on the surrounding fluid during the ciliary recovery phase because periciliary fluid viscosity is much lower than that of mucus gel. In addition, the no-slip condition along the epithelial surface also retards retrograde movement. Mucus viscosity and the presence of surrounding cilia further retard any retrograde mucus movement such that gravity has little effect on tracheobronchial mucociliary transport.
Derangement of metachronal motion impedes mucosal movement and increases the risk of disease or injury. Slowing mucosal velocity increases residence times in the affected airway region, permitting greater diffusion of deposited pathogens and toxins through periciliary fluid and increasing the risk of direct injury to airway epithelium and systemic injury via the bloodstream. Reducing the number, activity, or coordination of adjacent cilia or ciliary fields, hypersecretion of serous fluid or mucus gel, increased periciliary or mucus viscosity, and excessive periciliary fluid evaporation can each adversely affect mucociliary transport. Inspiring dry or cold air or cigarette smoke decreases periciliary fluid depth (altering cilia penetration into mucus gel) and cilia beat frequencies, which slows mucociliary transport. In addition, changes in periciliary fluid pH, ion concentration, or viscosity due to deposited chemicals, microorganisms (e. g., influenza, mycoplasmas), or systemic disease (e. g., asthma, cystic fibrosis) also inhibit ciliary beat frequency.
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