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The limbic
system appears to play an important role in the processing of
respiratory information, but the technology available to map cerebral
activation requires very circumscribed stimuli and is, thus far,
unsuitable for assessing relatively "messy" stimuli
as is found in most clinical situations such as the patient with
COPD. For example, in patients with emphysema the following conditions
may all play a role in the breathing discomfort: airway resistance,
hyperinflation, hypoxia, hypercapnia, and peripheral muscle and
cardiovascular deconditioning . With the exception of the chemoreceptors
and their role in mediating the responses to hypoxemia, hypercapnia,
and acidemia, our understanding of the neurological pathways responsible
for respiratory sensations remains relatively crude.
Given the absence of
discrete, well-defined neurological pathways to explain dyspnea,
and the complexity of the factors that contribute to respiratory
discomfort in most disease states, it seems reasonable to model
the disease in a way that one can control the number of variables
and isolate a single mechanism for study. A variety of breathing
devices have been employed to create resistive and elastic loads
on the respiratory system to mimic disease states. For example,
individuals with mild asthma are asked to breathe on external
resistors to mimic airflow obstruction. They are then asked to
describe their respiratory sensations. Subsequently, they inhale
methacholine to provoke bronchoconstriction.
Question
8.2
The sensations associated
with the external resistive loads are comparable to bronchoconstriction
in which of the following ways:
 | The
same sensations |
 | Different
but overlapping sensations |
 | Completely
different sensations |
Designing appropriate
models to study dyspnea is a considerable challenge, and one must
be cautious abut the limitations of the model when interpreting
results to explain clinical observations.
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