Journal of Applied Physiology
Vol. 83, No. 2, pp. 331-332, August 1997

Invited Editorial on "Airway thermal volume in humans and its relation to body size"

E. R. McFadden Jr.

Division of Pulmonary and Critial Care Medicine, University Hospitals of Cleveland, and Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio 44106

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THE STUDY OF AIRWAY THERMAL EVENTS has been an ongoing process for almost one-half of a century (18). It is an area of physiology that has been characterized by starts and stops, and major advances have come only slowly. For example, thirty years passed between the fundamental observations that the airways played a critical role in heating and humidifying the inspired air (2, 18) and the findings that this activity was really a distributed function that was not confined to the nose, mouth, and posterior pharynx (11). The early workers reached erroneous conclusions because their experiments were conducted primarily under resting conditions, rather than spanning the thermodynamic extremes to which the lungs are normally exposed. When this was rectified, it was found that whenever ventilation rises, unconditioned air readily moves from the extrathoracic to the intrapulmonic airways, and contact with as many as 10-15 generations of bronchi may be required to complete the conditioning process (11). Equally importantly, hyperpnea is invariably associated with a rise in respiratory heat exchange and a fall in the temperatures of the bronchial wall (3, 8, 11, 16). The only exception being when air at body conditions of temperature and water content is inhaled. The depth of penetrance and the temperature drop at any given site vary with the level of ventilation and the heat content of the inspirate. The greater the airflow and the colder and drier the air, the larger the changes.

These observations quickly spurred other investigations, and it soon became apparent that the cyclic cooling and rewarming with respiration represented a well-regulated exchange process that was linked to the local blood supply. Breath holding (8), cessation of hyperpnea (4-6), and the movement of blood into the thorax from the lungs during hyperventilation (7) are all associated with rapid rises in airstream temperatures, indicating the presence of an exogenous heat source that was most likely circulatory in origin (4-7). Such data also raised the theoretical possibility of using regional thermal fluxes as a means of quantitatively determining perfusion (8, 17).

Serikov and associates (Ref. 14; see p. 668 in this issue) have cleverly focused these observations to develop a means of measuring cardiac output in intubated patients without invading either the heart or the pulmonary circulation. Based on a lumped heat-capacity model, these authors reasoned that blood flow was the primary determinant of the temperature fluctuations that could develop in the trachea under certain circumstances, and from their calculations they derived a coefficient of transfer representing total lung heat capacity, which they termed "airway thermal volume" (ATV). In a series of elegantly simple experiments in which step decreases in the humidity of inspired gas were used to cool the airways, a strong correlation was found between the inverse of the exponential function describing the fall in airstream temperature and the standard clinical estimates of cardiac output. These investigators then successfully related ATV and body size and finally noted a significant direct linear relationship between standard estimates of blood flow and those derived from calculations of ATV. The method is technically simple, accurate, readily obtainable in any intubated individual, and obviates the need for right-sided cardiac catheterization in acutely ill patients.

Like all new advances, the concept is exciting, but there are issues that remain to be solved before the technique can be widely applied. The authors' model conceptualizes the bronchial tree as being surrounded by the pulmonary circulation, with the latter being the dominant heat source. Hence, in their eyes, fluctuations in tracheal blood flow mirror changes in central cardiac output. Their model also suggests, and their data confirm, that the key element (i.e., the reciprocal of the time constant of the temperature fall) is not materially influenced by the levels of ventilation employed. Both of these events certainly seem to be true in the resting state, but it remains to be determined whether they accurately reflect the system when it is placed under additional thermal stresses. As will be developed below, a simple event such as hyperventilation induces profound alterations in the intrathoracic milieu that may place limits on the circumstances in which this approach can be effectively utilized.

Controversy exists as to whether the heat provided to the airways is delivered from the bronchial or pulmonary vasculature (10, 15). Few would quarrel that the bronchial circulation reflects overall cardiac output at rest, but it is not established that this is the case when the intrathoracic and intrapulmonic airways are called on to condition the inspired air. This is a critical point that may become important whenever ventilation rises. There is now compelling evidence that the bronchial microvasculature, like the vessels in the skin, is responsive to thermal stimuli and that local blood flow in the airway walls can be regulated independently of left ventricular output (1, 4-6, 9, 12, 13). Voluntary hyperventilation as well as the hyperpnea of exercise are associated with important augmentations in bronchial perfusion in humans and animals that are sensitive to the same variables that promote heat loss (1, 9, 12). The colder and drier the air, and the higher the level of ventilation, the greater the change in blood flow. In addition, constriction or dilatation of the mucosal vessels influences the rate of cooling and rewarming for a given level of cardiac output (6). Equally importantly, hyperpnea, per se, also has been documented to influence the speed at which heat leaves and is resupplied to the bronchi (6, 16). This phenomenon may not have been seen in the present work because of the minimal ventilations studied. The authors noted significant differences between trials, but the absolute values were still little more than basal levels. Finally, some diseases like asthma are characterized by different rates of rewarming (4). These considerations may mean that there is an optimum range of ventilation and unique subject populations that will ultimately determine the selectivity and specificity of the measures developed. Future research should be most interesting, for it will allow us to take full advantage of the new opportunities provided by these resourceful investigators.

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