Disscusion about Conscious Perception of Bronchospasm as a Protective Phenomenon in Asthma

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Both neural and chemically mediated events contribute to the ventilatory responses seen when external loads are added to a subject’s breathing. The responses to internally loaded breathing cannot yet be studied in such a pure form. Thus, in our attempts to quantify the relationships between an internally added load and a subject’s awareness of the load, a number of compromises were accepted.

The subjects were part of a well-motivated group of outpatients and hospital staff, agreeing to undertake bronchoprovocation tests on a number of occasions. They were not apprehensive about the procedures, and while a conditioned response could not be ruled out, emphasis was placed on the explanation that the sequence of aerosol administration was randomized (although in practice, it was not).
Asthma Attack

Experiments utilizing externally loaded breathing, have defined threshold loads as those detected on only 50 percent of the occasions presented. The present study has the disadvantage of a purely subjective determination of threshold, that of the asthmatic subject undergoing an attack; however, we have confirmed that the degree of pulmonary dysfunction during such induced thresholds is comparable to that when symptoms of similar degree arise spontaneously (unpublished data). We believe, then, that study of such internal loading is more appropriate to clinical extrapolation than study of external loading. Furthermore, while we describe an “internal load,” we are aware that our measurements of pulmonary function give only a limited indication of the mechanical changes seen during the attacks. The lack of data obtainable with more invasive procedures was offset by the advantages of having our subjects available for repeated studies.

Given these limitations, our results reveal the following trends. If the baseline pairs of data are considered, each subject remained asymptomatic, despite fluctuation of at least 25 percent in some indices of airway caliber or lung volume. It seems, then, that such gradual deterioration in pulmonary function need not necessarily be associated with the development of symptoms. The data do not allow us to define limits to the degree of gradual deterioration beyond which symptoms become apparent; however, it may be relevant that fluctuations of 25 percent or more in the baseline FEVi were not seen in these subjects in the absence of symptoms. It is possible that this degree of gradual deterioration approximates the limits of change in pulmonary or airway mechanics beyond which symptoms will develop.

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A general pattern also emerges after consideration of the changes in percentages in the indices of pulmonary function needed to attain a threshold point from the asymptomatic state. The majority of pairs of data suggested that as baseline static lung volume increased and indices of airway caliber revealed greater airway obstruction, relatively smaller acute fluctuations were required to produce just noticeable symptoms.

We interpret these trends as confirming the clinical impression that gradual deterioration in pulmonary function need not necessarily be associated with the development of symptoms; however, superimposed on this adaption to gradual change is a greater awareness of acute deterioration in pulmonary function. Nevertheless, these conclusions should be considered in the light of the following two points.

First, in our comparisons of pairs of data, we have used absolute Raw, rather than the more common index specific airway resistance (ie, Raw/thoracic gas volume). We have also considered absolute Vmax50 uncorrected for alterations in lung volume. Our reasons are these. The FRC and Raw were the indices measured at the lung volume present when symptoms developed. These measurements, furthermore, did not require forced or maximal respiratory maneuvers. Since each independently provides information about the resistive and elastic components of the induced load, we considered that each should be compared in isolation. Our reasoning was similar in our use of Vmax50 as an index of resistive load, rather than the more commonly reported indices of Vmax at a nominated lung volume. Consider the following hypothetic example: A subject, initially asymptomatic and with normal pulmonary function, develops acute asthma, with his FRC increasing to the level of his recently normal TLC. Let us assume also that Vmax is important to the subject as an indicator of whether pulmonary dysfunction is present During the attack, VmaxFRC is sensed and may well be compared to a similar index recently remembered as being normal (VmaxFRC prior to the attack), not to a volume-corrected comparison (eg, VmaxTLC before the attack).

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Change in Pulmonary Function

Secondly, we have assumed that the percentage of change from baseline is an indicator of a subject’s “sensitivity to change in pulmonary function.” This may not be biologically appropriate. It may be that a subjects “sensitivity” should be considered in relationship to his maximal tolerable level of pulmonary dysfunction, ie, the nearer this limit is approached in the absence of symptoms, the less sensitive the subject (quite a different scale to our assessment using only one extreme of a ‘load spectrum”). While this approach is possible in some situations, the present study certainly precludes such an approach; however, we are able to compare our results to prior studies quantifying some respiratory sensations.

Some studies have suggested that respiratory sensations behave in accord with the Power law. This concept, validated for a variety of sensory modalities, compares the intensity of the stimulus to intensity of response. The log-linear relationship between the two seems generally accepted; however, our method does not allow comparisons with this concept.

Other authors have suggested that respiratory sensations may behave in accord with the Weber-Fechner law. Wiley and Zechman found that regardless of subjects’ initial level of pulmonary resistance, the addition of a constant proportion of this value was required in order to produce a threshold awareness of loading; however, comparisons were not made in the one subject with fluctuating baseline values for pulmonary function.

Other studies, using yet different methods, contrast to both of the previously discussed concepts. Perhaps the closest comparison to the present study was that of Aitken et al, as discussed by Wood. Their asthmatic subjects complained of more severe symptoms than did a group of normal subjects after the addition of a standard resistive load to breathing. Wood considered that the asthmatic subjects whose pulmonary function was already impaired were more sensitive to the added load than the normal subjects, a finding interpreted as contrasting to the expectations of the Weber-Fechner law, since the added load was a smaller proportion of the baseline load in the asthmatic subjects.

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Our results similarly contrast to the form of analysis described by the Weber-Fechner law. In attempting to separately analyze various mechanical components of our total “internal load,” we suggested that in any one subject, perception of added load was not constant; ie, there was a tendency for “greater sensitivity” to acute deterioration in pulmonary function at times when baseline pulmonary function was already impaired. It may be that such conscious awareness of acute deterioration in pulmonary function serves as a protective mechanism. Hudgel and Weil have documented a tendency for reduced ventilatory responses to hypoxia and hyper-capnia in subjects during intervals of remission of severe asthma. If this depressed ventilatory response is of importance in the development of respiratory failure precipitated by acute airway obstruction, a protective phenomenon at the level of consciousness might assume significance. This conscious perception of disease should certainly not be compromised by the practice, now sufficiently condemned, of administering sedatives to subjects suffering from acute asthma.