Dyspnea Definition

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					Dyspnea Definition

Dyspnea, a major cause of distress and disability in cardiac patients, is one of the most important
symptoms of heart disease. Yet it is one of the least understood, partly because it is inherently
subjective in nature and hence difficult to measure and partly because no single class of receptors,
discrete pathway, or mechanism has been found that can account for dyspnea in all the myriad
settings in which it occurs. Indeed, despite many decades of investigation summarized in several
excellent symposia, there is not even universal agreement concerning the definition of dyspnea,
although it is commonly regarded as "shortness of breath or an unpleasant intrusion of the normally
subconscious sensation of breathing into the conscious domain. It is most commonly seen in
patients with disease of the heart or lungs and in patients with mechanical dysfunction of the
respiratory apparatus, including the lungs, chest wall, and respiratory muscles.

Most would agree that in such patients shortness of breath at rest or during low-level muscular
exercise constitutes dyspnea. It is less obvious whether the term dyspnea could also be applied to
the respiratory distress experienced by normal individuals during maximal or near-maximal exercise
or at the break point of a breath hold. In these cases the term breathlessness is often used. Whether
the sensation is labeled "dyspnea" or "breathlessness" may depend on whether it is perceived as
appropriate or inappropriate to the level of activity. In the case of dyspnea, the respiratory distress
seems disproportionate to the degree of activity, and thus is considered pathologic, whereas in
breathlessness the sensation is appropriate to the respiratory demands, as in heavy exercise. A few
other terms should be defined at the outset.

These include hyperpnoea, the classic response to exercise, in which ventilation increases according
to metabolic demands, and, as a result, blood gas tensions, particularly CO2 tension, remain
constant. Hyperventilation, in contrast, refers to increases in ventilation that are dis-proportionate
to metabolic demands and thus lead to decreases in arterial CO2 tension. Tachypnea denotes a shift
in respiratory pattern to an increased respiratory rate and a decreased tidal volume. All of these
objective aspects of ventilation are frequently associated with dyspnea, but, unlike dyspnea, they
constitute measurable signs.

Dyspnea is in many respects analogous to pain: both are symptoms produced by noxious stimuli,
both are subjective warnings that something is wrong, and both may be protective. Pain serves to
limit motion in an injured extremity, and dyspnea may serve to limit exertion, thus preserving the
balance of gas exchange and metabolic demand. It may also minimize respiratory muscle fatigue.
Finally, dyspnea may be a factor in a feedback loop that results in optimal respiratory breathing
strategies that, in turn, reduce dyspnea—an analog of the way in which pain in an extremity may
lead a person to alter his gait to minimize pain. Unlike pain, however, dyspnea has thus far not been
associated with any single class of stimuli or receptors, nor have discrete pathways or central
nervous system (CNS) centers analogous to those mediating pain been described for dyspnea.
Indeed, a unifying theory that accounts for stimuli, pathways, and mechanisms of dyspnea and that
satisfactorily explains how and why dyspnea arises in so many clinical settings has not been found.
Still, a pathogen etic scheme can be formulated that explains many of the characteristics of dyspnea
and is helpful in understanding its features.

Respiratory Dysfunction
Ventilatory dysfunction leading to decreased ventilatory capacity is common to a large proportion of
patients complaining of dyspnea. Dysfunction can be due to increased airways resistance, as in
airways obstruction; to decreased lung compliance, as in restrictive lung disease; to changes in the
shape or compliance of the chest wall; to weakness of the respiratory muscles; or to inefficient
ventilation caused by alterations in dead space or ventilation-perfusion imbalance.

Ventilatory Capacity-Demand Imbalance
It is clear that, in addition to dysfunction of the respiratory apparatus, other factors must be
considered as, for example, in the case of a patient who breathes easily at rest but in whom
profound dyspnea is induced by mild exercise. Hypoxia, hypercapnia, and acidosis, which act to
increase ventilation, elicit a similar sensation, which suggests that dyspnea is more the result of an
unfavorable relationship between ventilatory capacity and ventilatory demand than of decreased
capacity alone. Decreased capacity may be well tolerated when ventilatory demands are low but
may lead to dyspnea in the face of even modest increases in ventilatory requirements.

Exercise is by far the most common stress leading to increased dyspnea in patients with respiratory
dysfunction, and it should be regularly inquired about during history taking. The answers to
questions about, for example, how many flights of stairs the patient can climb or the distance he or
she can walk on level ground before experiencing disabling dyspnea provide useful semi quantitative
information. In addition to exercise, a number of other ventilatory drives may also work to increase
ventilatory demand and contribute to the development of dyspnea. These include hypoxemia, which
may result from lung disease or from sojourn at high altitude, and acidosis, either respiratory or
metabolic, which is a classic stimulus to breathing and may precipitate or augment dyspnea in
patients with respiratory dysfunction.

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