Dyspnea, Orthopnea, and Paroxysmal Nocturnal Dyspnea
ABSTRACT Dyspnea refers to the sensation of difficult or uncomfortable breathing. It is a subjective experience perceived and reported by an affected patient. Dyspnea on exertion (DOE) may occur normally, but is considered indicative of disease when it occurs at a level of activity that is usually well tolerated. Dyspnea should be differentiated from tachypnea, hyperventilation, and hyperpnea, which refer to respiratory variations regardless of the patients" subjective sensations. Tachypnea is an increase in the respiratory rate above normal; hyperventilation is increased minute ventilation relative to metabolic need, and hyperpnea is a disproportionate rise in minute ventilation relative to an increase in metabolic level. These conditions may not always be associated with dyspnea. Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing. Paroxysmal nocturnal dyspnea (PND) is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position. Two uncommon types of breathlessness are trepopnea and platypnea. Trepopnea is dyspnea that occurs in one lateral decubitus position as opposed to the other. Platypnea refers to breathlessness that occurs in the upright position and is relieved with recumbency.
Dyspnea, Orthopnea, and
Paroxysmal Nocturnal Dyspnea
Dyspnea refers to the sensation of difficult or uncomfortable
breathing. It is a subjective experience perceived and re-
ported by an affected patient . Dyspnea on exertion (DOE)
may occur normally, but is considered indicative of disease
when it occurs at a level of activity that is usually well tol-
erated. Dyspnea should be differentiated from tachypnea,
hyperventilation, and hyperpnea, which refer to respiratory
variations regardless of the patients' subjective sensations .
Tachypnea is an increase in the respiratory rate above nor-
mal ; hyperventilation is increased minute ventilation relative
to metabolic need, and hyperpnea is a disproportionate rise
in minute ventilation relative to an increase in metabolic
level. These conditions may not always be associated with
Orthopnea is the sensation of breathlessness in the recum-
bent position, relieved by sitting or standing . Paroxysmal
nocturnal dyspnea (PND) is a sensation of shortness of breath
that awakens the patient, often after 1 or 2 hours of sleep,
and is usually relieved in the upright position .
Two uncommon types of breathlessness are trepopnea
and platypnea. Trepopnea is dyspnea that occurs in one lat-
eral decubitus position as opposed to the other. Platypnea
refers to breathlessness that occurs in the upright position
and is relieved with recumbency .
A patient with dyspnea may say : "I feel short of breath,"
"I'm having difficulty breathing," "I can't catch my breath,"
"I feel like I'm suffocating ." Because it is a subjective phe-
nomenon, the perception of dyspnea and its interpretation
vary from patient to patient . Begin with a nonleading ques-
tion: Do you have any difficulty breathing? If the response
is affirmative and dyspnea is established as a problem, it
should be characterized in detail . When did it begin? Has
the onset been sudden or insidious? Inquire about the fre-
quency and duration of attacks. The conditions in which
dyspnea occurs should be ascertained. Response to activity,
emotional state, and change of body position should be
noted. Ask about associated symptoms : chest pain, palpi-
tations, wheezing, or coughing. Sometimes a nonproductive
cough may be present as a "dyspnea equivalent ." What other
significant medical problems does the patient have, and
what medications has he been taking? How much has he
Dyspnea on exertion is by no means always indicative of
disease. Normal persons may feel dyspneic with strenuous
exercise. The level of activity tolerated by any individual
depends on such variables as age, sex, body weight, physical
conditioning, attitude, and emotional motivation . Dyspnea
on exertion would be abnormal if it occurred with activity
that is normally well tolerated by the patient. It is helpful
to ask if he has noticed any recent or progressive limitation
in his ability to conduct specific tasks that he was able to
perform without difficulty in the past (e.g ., walking, climb-
ing stairs, performing household chores) . The degree of
functional impairment can be assessed in this manner
Additional questions should be aimed at ascertaining
whether the patient has orthopnea or paroxysmal nocturnal
dyspnea. Inquire about the number of pillows he uses under
his head at night and whether he has ever had to sleep
sitting up. Does he develop coughing or wheezing in the
recumbent position? Did he ever wake up at night with
shortness of breath? How long after lying down did the
episode occur, and what did he do to relieve his distress?
Characteristically, the patient with left ventricular failure
sits up at bedside, dangles his feet, and refrains from am-
bulation or other activity that is likely to worsen his symp-
Spontaneous respiration is controlled by neural and chem-
ical mechanisms. At rest, an average 70 kg person breathes
12 to 15 times a minute with a tidal volume of about 600
ml. A normal individual is not aware of his or her respi-
ratory effort until ventilation is doubled, and dyspnea is not
experienced until ventilation is tripled . An abnormally in-
creased muscular effort is now needed for the process of
inspiration and expiration . Because dyspnea is a subjective
experience, it does not always correlate with the degree of
physiologic alteration. Some patients may complain of se-
vere breathlessness with relatively minor physiologic change ;
others may deny breathlessness even with marked cardio-
pulmonary deterioration .
There is no universal theory that explains the mechanism
of dyspnea in all clinical situations. Campbell and Howell
(1963) have formulated the "length-tension inappropriate-
ness theory," which states that the basic defect in dyspnea
is a mismatch between the pressure (tension) generated by
respiratory muscles and the tidal volume (change of length)
that results . Whenever such disparity occurs, the muscle
spindles of the intercostal muscles transmit signals that bring
the act of breathing to the conscious level . Additionally,
juxtacapillary receptors U-receptors), located in the alveolar
interstitium and supplied by unmyelinated fibers of the va-
gus nerve, are stimulated by pulmonary congestion . This
activates the Hering-Breuer reflex whereby inspiratory ef-
fort is terminated before full inspiration is achieved, re-
DYSPNEA, ORTHOPNEA, AND PAROXYSMAL NOCTURNAL DYSPNEA
suiting in rapid and shallow breathing. The J-receptors may
be responsible for dyspnea in situations where pulmonary
congestion occurs, such as with pulmonary edema . Other
theories that have been proposed to explain dyspnea in-
clude acid-base imbalance, central nervous system mech-
anisms, decreased breathing reserve, increased work of
breathing, increased transpulmonary pressure, fatigue of
respiratory muscles, increased oxygen cost of breathing,
dyssynergy of intercostal muscles and the diaphragm, and
abnormal respiratory drive .
Orthopnea is caused by pulmonary congestion during
recumbency . In the horizontal position there is redistri-
bution of blood volume from the lower extremities and
splanchnic beds to the lungs . In normal individuals this has
little effect, but in patients in whom the additional volume
cannot be pumped out by the left ventricle because of dis-
ease, there is a significant reduction in vital capacity and
pulmonary compliance with resultant shortness of breath .
Additionally, in patients with congestive heart failure the
pulmonary circulation may already be overloaded, and there
may be reabsorption of edema fluid from previously de-
pendent parts of the body . Pulmonary congestion decreases
when the patient assumes a more erect position, and this is
accompanied by an improvement in symptoms .
Paroxysmal nocturnal dyspnea may be caused by mech-
anisms similar to those for orthopnea . The failing left ven-
tricle is suddenly unable to match the output of a more
normally functioning right ventricle; this results in pul-
monary congestion . Additional mechanisms may be re-
sponsible in patients who experience paroxysmal nocturnal
dyspnea only during sleep. Theories include decreased re-
sponsiveness of the respiratory center in the brain and de-
creased adrenergic activity in the myocardium during sleep
Dyspnea on exertion is caused by failure of the left ven-
tricular output to rise during exercise with resultant in-
crease in pulmonary venous pressure. In cardiac asthma,
bronchospasm is associated with pulmonary congestion and
is probably precipitated by the action of edema fluid in the
bronchial walls on local receptors. Trepopnea may occur
with asymmetric lung disease when the patient lies with the
more affected lung down because of gravitational redistri-
bution of blood flow. It has also been reported with heart
disease when it is probably caused by distortion of the great
vessels in one lateral decubitus position versus the other
Platypnea was originally described in chronic obstructive
pulmonary disease and was attributed to an increased wasted
ventilation ratio in the upright position. Platypnea in as-
sociation with orthodeoxia (arterial deoxygenation in the
upright position) has been reported in several forms of
cyanotic congenital heart disease . It has been proposed that
this is precipitated by a slight decrease in systemic blood
pressure in the upright position, resulting in increased right-
to-left shunting .
Dyspnea may be induced in four distinct settings : (1) in-
creased ventilatory demand such as with exertion, febrile
illness, hypoxic state, severe anemia, or metabolic acidosis;
(2) decreased ventilatory capacity such as with pleural ef-
fusion, pneumothorax, intrathoracic mass, rib injury, or
muscle weakness; (3) increased airway resistance such as
with asthma or chronic obstructive pulmonary disease ; and
(4) decreased pulmonary compliance such as with interstitial
fibrosis or pulmonary edema .
In early left ventricular failure, the cardiac output does
not increase sufficiently in response to moderate exercise ;
tissue and cerebral acidosis occurs, and the patient expe-
riences dyspnea on exertion . The shortness of breath may
be accompanied by fatigue or a sensation of smothering or
sternal compression . In the later stages of left ventricular
failure, the pulmonary circulation remains congested, and
dyspnea occurs with mild exertion. Moreover, the patient
may develop orthopnea or paroxysmal nocturnal dyspnea .
Acute pulmonary edema is the most dramatic manifestation
of pulmonary venous overload and may occur in the setting
of a recent myocardial infarction or in the last stage of
chronic left ventricular failure . Cardiovascular causes of
dyspnea include valvular diseases (particularly mitral ste-
nosis and aortic insufficiency), paroxysmal arrhythmia (such
as atrial fibrillation), pericardial effusion with tamponade,
systemic or pulmonary hypertension, cardiomyopathy, and
myocarditis . Unrestricted fluid intake or administration in
a patient with oliguric renal failure is also likely to precip-
itate pulmonary congestion and dyspnea.
Pulmonary disease constitutes another major category of
conditions producing dyspnea and is discussed in Chapter
36. Important pulmonary causes include bronchial asthma,
chronic obstructive pulmonary disease, pulmonary embo-
lism, pneumonia, pleural effusion, pneumothorax, allergic
pneumonitis, and interstitial fibrosis. In addition, dyspnea
may occur in febrile and hypoxic states and in association
with some psychiatric conditions such as anxiety and panic
disorder. Diabetic ketoacidosis seldom causes dypsnea but
commonly induces slow, deep respirations termed Kussmaul
breathing. Cerebral lesions or intracranial hemorrhage may
be associated with intense hyperventilation and sometimes
irregularly periodic breathing called Biot's respiration . Ce-
rebral hypoperfusion from any cause may also result in
alternating periods of hyperventilation and apnea called
Cheyne-Stokes respiration, although no breathing difficulty
may be perceived by the patient .
Diagnosis of the cause of dyspnea can be made relatively
easily in the presence of other clinical signs of heart or lung
disease. Difficulty is sometimes encountered in determining
the precipitating cause of breathlessness in a patient with
both cardiac and pulmonary conditions. An additional di-
agnostic problem may be the presence of anxiety or other
emotional disorder. A careful history and physical exami-
nation are always helpful, and occasionally cardiac cathe-
terization, pulmonary function studies, or other tests may
be necessary .
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II.THE CARDIOVASCULAR SYSTEM
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