Airway Heat and Water Vapor Transport

5.2.5.1Longitudinal and Radial Temperature/Humidity Gradients

Air passing through the respiratory tract must be properly conditioned (warmed and humidified) in order to optimize alveolar 02 and C02 transport and minimize heat and water losses from the body. Respiratory air conditioning, as shown in Fig. 5.25, occurs as the airstream passes over the airway mucosal surfaces and results in both spatial and temporal humidity and temperature changes during each phase of respiration.37’38 Submucosal blood temperatures (TbioodJ are thought to be cooler in the extrathoracic airways and gradually warm along the length of the conducting airways until body core temperature ( roughly 37 °C) is achieved within the bronchi. This longitudinal temperature gradient exists because ambient air temperatures are generally lower than Tcnre. Inspired air extracts heat and water from airway walls as it passes through the lu­men, warming the airstream and cooling the wall. The radial temperature gradi­ent lessens as the ever-warmer airstream moves along the airway, causing gradually less heat extraction from the wall until eventually no hear is ex­changed. The process is reversed during expiration. At the onset of inspiration, the walls of the airway are their warmest and approach end-expiratory airstream temperatures throughout most of the respiratory tract.38)39 Typically, inspired air

Start of inhalation	U O	IMid- Inhalation	U 40 O «J	End Inhalation
I Tm warm ^ Ta warm	§30 2 G Q. A ~ 20 5 I 10 N,	Ta cool s’ Tm cool	2 30 Qi E I20 Ј * 10	F ^ Tm cool I% I, n WiifTH IIP H TVwarm

40

K. 30 E

20

10

Airway distance

Airway distance

0 0.2 0.4 0.6 0.8 1.0 Airway distance

End Exhalation

0 0.2 0.4 0.6 0.8 1 Airway distance

0 0.2 0.4 0.6 0.8 1.0 Airway distance

0 0.2 0.4 0.6 0.8 1.0 Airway distance

FIGURE S.25 The relationship between the inspiratory and expiratory airstream front boundary and air. 7^. and wall. T„. temperatures as a function of nondimenslonal distance from the nares. Solid lines shown on the airway picture indicate respiratory fronts and arrows depict the direction of airflow. Qualitative tem­peratures indicate relative temperature gradients across front boundaries. The graph depicts airstream tem­peratures as a function of nondimensional distance along the airway while breathing normal room air. Nondimensional distance is distance from the nares (x) divided by overall airway length (i.).

Is cooler than this, creating a radial temperature gradient, such that the air within the airway lumen is cooler than the walls (Fig 5.25). A radial water vapor con­centration gradient also exists because air at the air-mucus interface (airway wall) is fully saturated,40 while inspired air has a lower absolute humidity due to its being at a lower temperature than the airway wall.

Under most circumstances, passage of relatively cool inspiratory air along the airway results in convective and evaporative cooling of the mucosa while warming and humidifying the inspired air.38’39 Airflow patterns caused by convoluted upper airway morphology augment heat and water vapor trans­port.41^4 Radial temperature gradients can persist at least as far as the carina during oral breathing of room air,45’46 causing heat and water vapor exchange to occur for much of the length of the upper airway. At the end of inhalation, longitudinal temperature and water vapor concentration gradients exist along the airway (Fig. 5.25). Air reaching the most distal airway regions (beyond about the fourteenth bronchial generation) is believed to be fully conditioned (37 °C, 100% humidity) during normal breathing. Exhalation causes warm air originating in the distal airway to pass over airway walls in proximal air­way segments, which had been cooled during inspiration and are normally maintained below body core temperature.47 The resulting temperature gradi­ent causes airstream water vapor to condense and the airstream to lose heat to the airway walls. This acts to minimize net heat and water losses.48

Effectiveness of the conditioning process is dependent upon respiratory tract geometry, ambient air temperature (Tarab) and humidity (Camt,), inspira­tory and expiratory flow rates and volumes,48 mucus temperature (7m), air­way wall blood temperature (Tblood), and flow rate in the submucosal capillary bed.49-52 These variables interact and their effects are interdependent. For ex­ample, airway geometry plays a major role in conditioning since the rate of heat exchange between the wall and airstream, q is given by

Q = bAsAT, (5.43)

Where b = heat transfer coefficient, As = airway wall surface area, and A7" = temperature difference between the airstream and wall.53 Water vapor ex­change is analogous to heat exchange and thus is also a function of As.54 In addi­tion, both mean gas velocity, u and residence time, tw, are dependent on airway geometry since tw = f(u), u = f(A), and conduit geometry directly affects the generation of flow disturbances and subsequent development of turbulent flow.

5.2.5.2 Role of Airway Heat and Water Vapor Exchange in Disease and Injury

Exchange of heat and water vapor in the respiratory tract can significantly influence airway patency, alveolar gas transport, and whole body homeostasis, such as seen with cold — or exercise-induced bronchospasms. Maintaining air­way patency is important in reducing airway resistance, maximizing inspira­tory volume, and minimizing the work of breathing. The mechanism by which heat and water vapor exchange influences airway resistance has been widely debated55-57 but probably depends on both airway mucosa heat and water losses.47’58 It has been suggested that alterations in the conditioning of inspired and expired air can lead to increased total airway resistance39’47’49’55 by causing increased nasal blood flow,59,60 altering vascular tone and permeability in the bronchial circulation,61 and increasing airway smooth muscle tension.6-"1’5 Un­der pathological conditions, diminished conditioning may also increase mucus thickness,17’66 which in extreme cases causes increased airway resistance by re ducing airway cross-sectional area and increasing shear stress at the air/mucus interface.67 In addition to effects on the conducting airways, alveolar 02 and C02 transport could be hampered if air has not been warmed to body temper­ature (37 °C) and fully humidified by the time it reaches the alveoli.

The importance of respiratory heat and water losses is not confined to the respiratory structures. Inspiration of cold, hot, or dry air poses the po­tential threats of thermal injury or desiccation to the airway epithelium46’52’66’68’69 and is a challenge to whole-body thermoregulation. Under certain conditions, such as hyperbaria,70’71 airway heat losses can account for a considerable percentage of total body heat production (in some cases > 100%).71 Normally these threats are ameliorated by rapid moderation of inspired air temperature and humidity by exchanging heat and water vapor between the mucus and airstream in the upper airway.72-74 Recovering much of the heat and water vapor contained in expired air minimizes heat and water losses to the ambient environment75 and aids in whole-body thermoregulation.

Heat and water vapor transport can also lead to respiratory impairment, in fection, and injury through thermal and osmotic stresses occurring at the mu­cosal epithelium.66’75 These stresses cause changes in mucus osmolarity, pH, ciliary activity, and cellular transport,73,76 resulting in altered mucosal thickness17’66 and impaired airway defenses. Normal breathing allows microor­ganisms, pollutant gases, and particulate matter to contact the mucus coating (comprised of mucus gel and periciliary fluid) atop the apical surface of respira­tory epithelium. A complex system of chemical, immunological, and mechanical defense mechanisms protects the respiratory epithelium and alveoli from poten­tial diseases or injury caused by noxious airstream components.77 Aside from chemical neutralization of pollutants in the airstream78’79 and physical defenses such as bronchoconstriction, coughing, and particle impaction caused by airwray morphology,77’80-82 the defense of the airway depends on the physical and chemical properties of airway mucus (e. g., chemical detoxification reactions with proteins83) and the ciliary mechanism which moves it toward the epiglottis (mucociliary escalator). Inspiring cold dry air can impede mucociliary transport, reducing mucus velocity and increasing the risk of airway disease or injury.

Airway deposition patterns of inspired hygroscopic particles are also af­fected by airway heat and water vapor exchange. Inspired particles passing from a relatively dry ambient environment into the fully saturated airway quickly adsorb water from the surrounding airstream. Water vapor adsorption at the particle surface increases hygroscopic particle mass mp as a function of particle diameter dg and the water vapor concentration gradient between the bulk fluid, and particle surface, c0, according to

= 2 TrdgDw Cw(- c0), (5.44)

Where Dw — diffusion coefficient of water vapor in air and Cw = slip correction factor = f(dg, Du„ T).84 In addition, dg can be determined from mp and particle density, p,

1/3

Ds = 1

4ttp(X)

3 m-,

(5.45)

Where X = particle composition at time Ј.85 Particle growth continues until equilib­rium is reached between particle surface and bulk airstream water vapor pressure. Given sufficient growth, extremely fine particles that might otherwise pass entirely through the airway during the breathing cycle deposit along the airway because of the increase in mass. Compromised extrathoracic submucosal blood flow due to in­jury or disease will change water vapor exchange between the mucosa! surface and inspired airstream. This in turn will alter the growth patterns of inspired hygro­scopic particles. This process may play a role in lower airway injury caused by in­spired toxins (e. g., acid aerosols) or succumbing to diseases normally present in the ambient environment (e. g., pneumonia) that seem to affect weakened individuals.

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