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If we
have normal respiratory and cardiovascular systems, we develop
respiratory discomfort when we push ourselves to our physical
limits during exercise. Our level of "fitness" determines
how far we can go. Fitness reflects the ability of the heart to
increase cardiac output and the ability of the peripheral muscle
to utilize oxygen for the purpose of aerobic metabolism during
exercise. The latter is dependent upon the level of oxidative
enzymes present in the muscle, a quantity that increases with
physical training and diminishes with a sedentary lifestyle. Stimulation
of metaboreceptors may mediate the respiratory discomfort experienced
in this setting. Patients with chronic diseases not infrequently
curtail their physical activity and become deconditioned. They
may then complain of dyspnea, which is often attributed to their
underlying disease but that is actually the consequence of diminished
fitness.
| Figure
16.1: The Dyspnea Spiral
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| Reprinted
from Haas F, Salazar-Schicchi J, Axen K. Desensitization
to dyspnea in chronic obstructive pulmonary disease. In: Casaburi
R, Petty TL, eds. Principles and Practice of Pulmonary
Rehabilitation. Philadelphia, PA, WB Saunders Company;1993:241-25. |
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The patient described
previously with enlarged left ventricle and dyspnea on exertion
illustrates a case in which a primary cardiovascular condition
is the cause of the dyspnea. The onset of wheezing after walking
a minimal distance is not characteristic of exercise-induced asthma.
Rather, it is more likely that the patient has a non-compliant
left ventricle from hypertrophic cardiomyopathy secondary to his
hypertension. With the stress of exercise, the heart attempts
to increase cardiac output leading to an acute rise in pulmonary
capillary wedge pressure, stimulation of pulmonary receptors and,
with passage of fluid into the lung, further stimulation of C-fibers
and the imposition of a load on the ventilatory pump due to cardiac-induced
bronchospasm.
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