Respiratory heat and water exchange: physiological and clinical implications

1983 ◽  
Vol 54 (2) ◽  
pp. 331-336 ◽  
Author(s):  
E. R. McFadden

Recent evidence demonstrates that the conditioning of inspired air is not confined to the upper airways as formerly thought but rather involves as much of the tracheobronchial tree as necessary to complete the process. As the need to condition more air is increased by raising ventilation and/or lowering inspired temperature (and so water content), the point at which the inspirate reaches body conditions moves progressively deeper into the lungs, and under extreme conditions thermal transfers can be measured in airways less than 2 mm in diameter. The decrease in airway temperature that develops from the movement of heat and water from the mucosa during inspiration not only facilitates recovery during expiration by reversing the thermal gradients, but it may also produce airway obstruction in susceptible individuals by an as yet undefined mechanism. Respiratory heat exchange may also interact with airway secretory processes and mucociliary transport mechanisms and may help regulate bronchial blood supply.

1979 ◽  
Vol 46 (3) ◽  
pp. 467-475 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
R. H. Strauss ◽  
J. J. Jaeger

We have hypothesized that it is the total heat flux in the tracheobronchial tree during exercise that determines the degree of postexertional obstruction in asthma, and have developed quanititative expressions that relate these two events. We tested this hypothesis by comparing the observed responses to exercise, while our subjects inhaled dry air at various temperatures ranging from subzero to 80 degrees C in a random fashion, to those that we predicted would occur based upon calculations of respiratory heat exchange. We further determined if heat could be transferred from the inspired air to the mucosa so as to offset evaporative losses from the airways. The observed responses fell as air temperature was increased from -11 to +37 degrees C and exactly matched theoretical predictions. Above 37 degrees C, the observed response exceeded predictions, indicating that it was not possible to provide sufficient heat per se in the air to offset the vaporization of water. However, when small amounts of water vapor were added to the inspirate at high temperatures, bronchospasm was virtually abolished and the response again closely matched theoretical expectations. We conclude that the magnitude of exercise-induced asthma is directly proportional to the thermal load placed on the airways and that this reaction is quantifiable in terms of respiratory heat exchange.


CHEST Journal ◽  
1984 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
W.C. Hodgson ◽  
D.J. Cotton ◽  
G.D. Werner ◽  
D.W. Cockcroft ◽  
J. A Dosman

1984 ◽  
Vol 57 (2) ◽  
pp. 608-609 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
J. J. Jaeger

Author(s):  
R D Farley ◽  
K R Patel

Exercise-induced asthma is prevalent in many asthmatics and during the winter months can be exacerbated by cold air inhalation. A laboratory facility was required to permit early diagnosis of cold air sensitivity in these patients. This paper describes the development of a modular air conditioning system to produce a range of inhalative thermal burdens and the microcomputer interfacing to measure the rate of airway heat loss imposed. A single-stage refrigerator was built capable of cooling 150 1/min air to —25°C. This was also used to generate dry ambient temperature air by rewarming the chilled air supply. An air humidifier was developed based upon natural convection and evaporation. It was capable of raising 150 1/min ambient air to 37°C, 100 per cent relative humidity. In two pilot studies of 18 asthmatics it was found that the rate of respiratory heat exchange could be correlated with the magnitude of post exertional bronchoconstriction (lung dysfunction) and that exercise-induced asthma could be minimized by attenuating the rate of airway heat loss.


2010 ◽  
Vol 132 (3) ◽  
Author(s):  
K. Bauer ◽  
H. Chaves ◽  
Ch. Brücker

The convective transport of fluid within the human upper airways is investigated in a transparent model of the tracheobronchial tree. Oscillatory flow through the branching network with six generations was studied at varying Reynolds numbers between 400 and 2600 and Womersley numbers from 5.5 to 12.3 in the trachea representing clinical conditions during high frequency oscillatory ventilation. The flow partitioning within the model was visualized using advection of neutrally buoyant tracer particles, which were illuminated by short light pulses and recorded by a high speed camera. Integration of the particle locations for a large number of cycles provides the probability distribution of particles passing certain branches within the bifurcating network, and thus, the dispersion of particles in the airways. The results show the different characteristics of flow partitioning at varying Womersley and Reynolds numbers.


2020 ◽  
Author(s):  
Susyn Joan Kelly ◽  
Paul Martinsen ◽  
Stanislav Tatkov

Abstract BACKGROUND: Inspired air is heated and humidified in the nose before it reaches lower airways. This mechanism is bypassed during tracheostomy, directly exposing the lower airways to colder and drier air from the environment, which is known to have negative effects on mucociliary transport; however, little is known about how quickly mucociliary transport deteriorates. The purpose of this study was to determine the short-term effect of flowing room air on mucociliary transport in the trachea. In an ovine perfused in vitro tracheal model (N=7) the epithelium was exposed to 25 L/min of flow, heated to lamb body temperature (38 °C) and fully saturated with water vapor as the control, followed by room air (22 °C and 50% relative humidity) for a short duration, until mucociliary transport had visually stopped. Mucus transport velocity (MTV) and cilia beat frequency (CBF), as well as the area of the surface with beating cilia, were continuously measured with video-microscopy.RESULTS: Exposing the tracheal epithelium to air heated to body temperature and fully humidified resulted in stable MTV 9.5 ± 1.1 mm/min and CBF 13.4 ± 0.6 Hz. When exposed to the flow of room air, MTV slowed down to 0.1 ± 0.1 mm/min in 2.0 ± 0.4 seconds followed by a decrease in CBF to 6.7 ± 1.9 Hz, after 2.3 ± 0.8 second. Both MTV and CBF recovered to their initial state when heated and humidified air-flow was re-introduced. CONCLUSIONS: This study demonstrates mucociliary transport can deteriorate within seconds of exposing the tracheal epithelium to flowing room air. The reduction in MTV precedes slowing of CBF. Their relationship is non-linear and a minimum CBF of approximately 6 Hz is required for MTV > 0. Clinically these findings indicate a potential rapid detrimental effect of breathing with non-humidified air via bypassed upper airways.


1981 ◽  
Vol 51 (5) ◽  
pp. 1287-1293 ◽  
Author(s):  
A. S. Slutsky

A quantitative theoretical model of the enhanced gas mixing secondary to cardiogenic oscillations is presented based on the concept of augmented gas transport within the tracheobronchial tree (Science 209: 609, 1980). The model assumes “well-mixed” flow in the upper airways with the enhanced mixing described by Deff = Dmol + K . ud, where Deff is the effective diffusivity; Dmol, the molecular diffusivity: K, a constant; u, the root-mean-square flow; and d, the airway diameter. In the smaller airways on analysis based on Taylor laminar dispersion is used described by Deff = Dmol + (1/192) (ud)2/Dmol. The model predicts that, in dogs, cardiogenic oscillations should enhance gas mixing about 10-fold depending on the flow rates generated by the heart. Other predictions are that the augmentation of gas mixing should be greater 1) at lower lung volumes, 2) with sulfur hexafluoride vs. helium or air, 3) after peripheral airway dilation, and 4) after central airways constriction. Theoretical predictions are very close to published experimental results where available. This model should help in the development of mathematical models of gas mixing within the lungs that will include the contribution of cardiogenic oscillations.


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