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Key points
Dyspnoea is the sensation of breathing discom-
fort that can be described with different terms
according to different pathophysiological
mechanisms that vary in intensity.
The mechanisms of dyspnoea are complex.
In COPD, whilst the intensity and quality of dys-
pnoea during activity correlates with the magni-
tude of lung hyperinflation and inspiratory
events, it correlates poorly with FEV1.
Valid, reliable and responsive instruments are
available to measure the severity of dyspnoea in
patients with respiratory disease.
measurement 1
Pulmonary Unit, Cardio-Thoracic
Dept, University-Hospital Pisa,
Pisa, and 2Clinica Medica,
CME article: educational aims University-Hospital Careggi,
Firenze, Italy.
perceived and described only by the individual dyspnoea is influenced by a mismatch between
who is experiencing it [2]. Despite this scientific the respiratory motor command from the CNS
relativism, this article tries to describe dyspnoea in and afferent feedback arising from the receptors
a scientific manner, in which it can be defined by (described previously) in the respiratory system
numeric characterisation, that is “to be able to (neuroventilatory dissociation (NVD) of the respi-
measure” [3]. ratory pump) [6–8]. In chronic obstructive
pulmonary disease (COPD) patients during exer-
cise, the relationship between effort (motor
Mechanism of output) and the anticipated ventilatory conse-
quence (instantaneous change in tidal volume) is
dyspnoea seriously disrupted, i.e. NVD, as a result of weak-
Receptors in the airways, lung parenchyma, re- ened or less effective inspiratory muscles due to
spiratory muscles and chemoreceptors provide dynamic hyperinflation (DH). Under these condi-
sensory feedback via vagal, phrenic and inter- tions, the patient experiences marked inspiratory
costal nerves to the spinal cord, medulla and difficulties. The psychophysical basis of NVD
higher centres [4]. probably resides in the complex central process-
Peripheral and central chemoreceptors can ing of integrated sensory information relative to:
sense changes in arterial oxygen tension, carbon 1) the level of central motor command output [9];
dioxide tension and pH. Indeed, in patients with and 2) instantaneous feedback from a number of
impaired ventilatory function, chronic respiratory respiratory mechanoreceptors that provide pro-
failure may be revealed by exercise and, therefore, prioceptive information.
may induce dyspnoea. This is reflected by changes
in blood gases during exercise, specifically when Other mechanisms
lung diffusion is impaired or alveolar dead space Dyspnoea may also result from a lack of increase
is increased. in the ejection fraction of the left ventricle.
Among the pulmonary receptors, slowly Dyspnoea can occur due to lactate production at
adapting stretch receptors, located principally in the skeletal muscle level. This acidosis can occur
the large airways, respond to increases in lung vol- at low levels of exercise, thus reducing the walk-
ume. Rapidly adapting receptors in the airway ing distance achievable by a patient and
epithelium respond to different stimuli, such as generating dyspnoea. Lastly, there are some
particulate irritants, direct stimulation of the air- aspects of the central processing at the CNS level
ways and pulmonary congestion. Juxta- that are potential contributors to the perception
pulmonary receptors are non-myelinated fibres of dyspnoea [10].
(C-fibres), that are located near pulmonary capil-
laries and in the bronchial and laryngeal mucosa,
and are stimulated by mechanical and chemical
stimuli. Almost all of the afferent signals from pul-
Language of
monary receptors are ultimately carried to the breathlessness
central nervous system (CNS) via the vagus nerve. Dyspnoea descriptors can help in the under-
Mechanical receptors for volume, flow, muscle standing of the language of dyspnoea [11–15].
shortening, muscle tension and chest wall dis- Nevertheless, differences in language, race, cul-
placement provide a peripheral sensory feedback, ture, sex and previous experience can all change
modulating the intensity of central motor output the perception and the manner that the feeling of
at the central sensory level. Dyspnoea may reflect being dyspnoeic is expressed to others [16–18].
the perception of effort; that is the awareness of For example, in a study in COPD patients [18], at
the efferent motor command from the CNS to the any given level of exercise, females were more
respiratory muscles. breathless than males. Vagal activity contributes
Dyspnoea may occur when a greater than to the sensation of “chest tightness”, a term fre-
expected respiratory muscle activity is required to quently reported by asthmatic patients, which
produce a given amount of ventilation. This has may arise from the stimulation of sensory recep-
been described as “length-tension inappropriate- tors within the lungs mediated through vagal
ness” [5]. With regard to the respiratory system, pathways [19]. Several clinical conditions are
“length” actually corresponds to the change in characterised by descriptors as “work/effort” [11].
lung volume, while “tension” corresponds to the The intensity of the motor command to ventila-
respiratory pressures produced. Intensity of tory muscles relayed to the sensory cortex
(corollary discharge), alone or in combination severe FEV1 decrease and hyperinflation [28].
with force generation and respiratory muscle con- Perception and descriptors of dyspnoea are also,
traction, can be perceived as a sensation of “effort” and more remarkably, important for the definition
and considered as difficult breathing [20, 21]. of asthma severity. It has been shown that
Patients with interstitial lung disease frequently patients suffering from near-fatal asthma (NFA)
use terms such as “rapid” and “shallow” to attacks have a blunted perception of dyspnoea
describe their respiratory discomfort [11, 12, 15, [29]. Patients with a low perception of dyspnoea
22]. Descriptions such as “air hunger”, “need to had statistically significantly more hospitalisa-
breathe” and “urge to breathe” appear to be relat- tions, NFA attacks and deaths during a follow-up
ed to an increased respiratory drive [13]. period [30]. In addition, it has been found that
perception of dyspnoea is blunted in NFA patients
both at rest and at the end-point of various exer-
Dyspnoea and cises [31]. In addition, the mechanisms involved
in the exercise limitation observed in NFA patients
specific diseases were different from those found in non-NFA sub-
jects: the former stopped exercising mainly
COPD because of leg discomfort, whereas the latter
Pathophysiological factors known to contribute to stopped predominantly because of dyspnoea
dyspnoea in COPD patients include: increased [31].
intrinsic mechanical loading of inspiratory mus-
cles, the inspiratory threshold load (the dynamic
intrinsic positive end-expiratory pressure (PEEPi)
Table 1 Descriptors for dyspnoea in different conditions
[23]); increased mechanical restriction of the tho-
Rapid breathing Chronic heart failure
rax; inspiratory muscle weakness; increased
Incomplete exhalation Asthma
ventilatory demand relative to capacity; gas Shallow breathing Restrictive diseases
exchange abnormalities; dynamic airway com- Increased work/effort COPD, interstitial lung disease, neuromuscular disease,
pression; cardiovascular factors; and any chest wall diseases
combination of the above [24]. Neither the forced Suffocation Chronic heart failure
expiratory volume in one second (FEV1) nor the Air hunger COPD, chronic heart failure
FEV1-to-vital capacity ratio are good predictors of Tight chest Asthma
dyspnoea in patients with severe chronic airflow Heavy breathing Asthma
obstruction. There is a close correlation between
hyperinflation (as demonstrated by reduction of
inspiratory capacity) during exercise and the Interstitial/restrictive lung
intensity of exercise dyspnoea [8, 9]. In contrast to disease
healthy subjects who report a perception of Patients with restrictive lung disease adopt a
increased effort/work at the end of exhaustive tightly constrained breathing pattern, probably
exercise, patients with COPD select descriptors of as a strategy for avoiding dyspnoea [32]. They fre-
inspiratory difficulty and unsatisfied inspiration quently complain of “work/effort”, “unsatisfied
(i.e. “can’t get enough air in”) [9]. During exercise, inspiration”, “inspiratory difficulty”, and “rapid”
COPD patients also report qualitative perceptions and “shallow” breathing [32–35]. These sensa-
of “unsatisfied” or “unrewarded” inspiration, “shal- tions have their physiological basis partially in an
low breathing” and “inspiratory difficulty”. These impaired ability to increase lung volume and dis-
distinct sensations are associated with DH and its place the thorax appropriately in the setting of an
negative mechanical effects, i.e. PEEPi and the increased ventilatory drive.
uncoupling of the normal association between
respiratory effort and ventilatory output [9, 25]. Congestive heart disease
Patients with chronic heart failure may stop exer-
Asthma cising because of intolerable exercise dyspnoea,
Patients describe spontaneous and induced asth- leg fatigue or both at a point where there is appar-
ma using similar terms [26, 27]. In induced ent cardiopulmonary reserve [36]. During
asthma, the initial sensation of “chest tightness” exercise, these patients describe their dyspnoea
reflects the breathing discomfort resulting from using the cluster “suffocating at rest “, “rapid
mild bronchoconstriction; the sensation of “work” breathing”, “air hunger” [9], a “need to sigh” [11],
or “effort” of breathing is experienced with a more or “work/effort” [14].
✘
scale [45] has been used extensively as a discrim-
inative instrument, based on the magnitude of
0 1 2 3 4 5 6 7 8 9 10 task that provokes dyspnoea (figure 3). The MRC
VAS Scale scale is simple to administer and correlates with
other dyspnoea scales and with scores of health
status [46]. It has been recently included in a
Category-ratio scale global index that is able to predict the risk of
The modified 0–10 category-ratio Borg scale is death from any cause and from respiratory
the most widely used scale to rate dyspnoea dur- causes among patients with COPD [47]. MRC and
ing exercise testing [40]. This scale consists of a other similar scales focus only on one dimension
vertical line labelled 0 to 10, with nonlinear spac- that affects dyspnoea; furthermore, the grades are
ing of verbal descriptors of severity corresponding quite broad, so that it may be difficult to detect
to specific numbers. The subject can choose the small but important changes with particular inter-
number or the verbal descriptor to reflect ventions [37].
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