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CHAPTER
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14
yspnea, or shortness of breath, is a subjective sensa-
D
tion of air hunger that results in labored breathing.
True dyspnea results from three general causes: (1) an
increased awareness of normal breathing, such as with
hyperventilation; (2) an increase in the work of breathing,
such as in airway obstruction or restricted volume; and
(3) abnormalities in the ventilatory system, such as in
neurological disorders, diseases of the muscles, and chest
wall abnormalities. In disease states it is usually a result
of pulmonary or cardiac pathology. When eliciting the
history, it is helpful to determine if this is new-onset acute
dyspnea, chronic progressive dyspnea, or chronic recurrent dyspnea. Carefully directed questioning will provide
essential clues for identifying the differential diagnosis.
In children younger than 3 years, who usually cannot express the sensation, caregivers can observe tachypnea,
retractions, stridor, nasal aring, or feeding difculty.
Dyspnea
DIAGNOSTIC REASONING: FOCUSED
HISTORY
Is this an emergency?
Severe dyspnea is a medical emergency. If not treated
immediately, respiratory failure and death can occur.
Assess the adequacy of the airway rst. Emergency
measures should be instituted to establish ventilation.
When the patient is stabilized, search for the underlying
cause of the dyspnea.
Key Questions
l
Did this occur suddenly or has it been developing
gradually? Over what period of time (hours, days,
weeks) has it developed?
l
What were you (or the child) doing just before having
difculty in breathing?
l
Do you (or the child) have other symptoms such as
itching or swelling?
Onset
New-onset acute dyspnea in a patient in respiratory
distress can signal a life-threatening problem. In the
patient with no previous history of heart or lung disease, dyspnea can indicate several conditions that
require immediate treatment such as aspiration of a
foreign body, anaphylaxis, pulmonary embolism (PE),
and pneumonia. A common cause of acute-onset dyspnea is left ventricular dysfunction.
Acute upper or lower airway obstruction in children has the greatest potential to cause serious morbidity or mortality and therefore must initially be
ruled out. The most serious problem is hypoxemia
caused by the inability to transport oxygen past a
blocked upper airway, such as with epiglottitis, croup,
or a foreign body.
Acute dyspnea requires immediate assessment of
the airway and ventilatory status with oxygen and cardiac monitoring. Often this must occur before a denitive diagnostic evaluation has been completed.
Acute epiglottitis in children is caused by Hae-
mophilus inuenzae. Inammation of the epiglottis
causes edema that obstructs the tracheal airway. The
onset is sudden and the course of the disease is rapid.
The patient’s presenting symptoms usually include
drooling, dysphonia, dysphagia, and respiratory distress with inspiratory stridor. The child looks anxious
and sits up and forward with the jaw open to assist in
air intake.
Status asthmaticus is a progressive bronchospasm
from an increase in airow resistance in children who
are having an asthma event that does not respond to
pharmacological intervention. Fever can be present,
and pulse rate and respirations are increased. The use
of accessory respiratory muscles is seen. Sometimes
wheezing is not heard because of lack of air movement. The combination of hypoxia, hypercapnia, and
acidosis can result in cardiovascular depression and
cardiopulmonary arrest.
Foreign Body Aspiration
The adult patient with foreign body aspiration reports that dyspnea occurred while eating solid foods
or drinking large amounts of alcohol. Children who
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Chapter 14 • Dyspnea
put small objects in their mouth are at risk for aspiration of the object into the airway and subsequent
airway obstruction. The patient or the care provider
gives a history of sudden onset of choking, coughing,
or wheezing without preceding upper respiratory
tract infection. Often the child has been playing
on the oor or outside at the time of the onset of
symptoms.
Anaphylaxis
Anaphylaxis can follow insect bites or the ingestion of
medication or other potential allergens (e.g., shellsh,
peanuts). Primary symptoms include ushing, generalized pruritus, anxiety, faintness, and sneezing. An
allergic response can lead to shock, cardiac arrhythmia, laryngeal edema, and death within minutes. Generally the sooner the symptoms occur, the more severe
the reaction.
Is the dyspnea caused by a secondary obstruction
in the lower respiratory tract?
Key Questions
l
Have you had a cough or recent cold?
l
Do you have a history of asthma?
l
Is there a family history of asthma?
Cough
Secondary partial airway obstruction caused by small
airway disease contributes to hypoxemia via intrapulmonary shunting. The pulmonary obstruction
can be intraluminal (distal foreign objects, asthma);
intramural (edema, bronchomalacia, bronchiolitis);
or extramural (compression from tumor, lymph
nodes). The narrowing increases both airway resistance and turbulence of airow. The imbalance between pulmonary ventilation and perfusion affects
oxygen exchange. This causes the patient to work
harder to maintain adequate ventilation, resulting in
dyspnea.
History of Asthma
Both adults and children can experience airway obstruction caused by reactive airways disease or asthma.
Personal or family history of asthma increases the risk
of dyspnea from acute bronchospasm.
Trauma
Limitation of motion of the thoracic cage because of
pain and/or trauma can be associated with severe alveolar hypoventilation and subsequent dyspnea.
Pneumothorax occurs most frequently in young
people during strenuous activity. Spontaneous pneumothorax results in sudden loss of lung volume, hypoxia, hypercapnia, and signicant shortness of breath.
Blunt chest trauma can be caused by a fall or motor
vehicle accident.
Is the dyspnea caused by a pulmonary embolus?
Key Questions
l
Have you recently been conned to bed or been sit-
ting for a long period of time?
l
Have you had recent surgery?
l
Have you recently sustained a fracture?
l
Are you taking birth control pills or estrogen?
l
Have you had any pain in your legs?
l
Do you have a history of deep vein thrombosis?
l
Do you have a family history of clotting disorders?
l
Do you smoke?
l
What medications are you taking?
l
Are you feeling anxious or scared?
The person with PE is usually in acute distress and
reports signicant shortness of breath, localized pleuritic chest pain, apprehension, bloody sputum production, diaphoresis, fever, and history of conditions that
increase risk for emboli. These risk factors include
age of greater than 60 years, pulmonary hypertension,
congestive heart failure, chronic lung disease, ischemic heart disease, stroke, and cancer. Predisposing
factors that can contribute to thrombus formation include (1) venous stasis, (2) hypercoagulability, and
(3) endothelial injury with inammation to the vessel
lining. Trauma, muscle spasm, or clot dissolution can
cause the thrombus to dislodge, creating an embolus.
Emboli circulate in the blood to the right side of
the heart and enter the lungs via the pulmonary
artery. If the clot is not dissolved within the lungs, it
occludes the pulmonary artery and obstructs blood
ow and perfusion of the lungs. Patients with suspected PE are referred for emergency pulmonary/
vascular consultation.
Is the dyspnea caused by trauma to the chest?
Key Question
l
Have you experienced any trauma to the chest?
Confinement, Surgery, and Fracture
People with a history of deep vein thrombosis or prolonged immobility are at greater risk for PE. Vascular
lung disease is characterized by a decrease in the size
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161
of the pulmonary vascular bed. When emboli reach
the pulmonary artery, the reduced blood ow through
the lungs results in arterial hypoxemia and hypercapnia. Hypoxemia and hypercapnia lead to symptoms of
dyspnea. Dyspnea resulting from PE is usually accompanied by fever, chest pain, and restlessness.
Family History of Clotting Disorders
Antiphospholipid syndrome, occurring either as an
isolated disorder or as a part of systemic lupus erythematosus, can lead to abnormal clotting. This has a hereditary component and can occur as a spontaneous
mutation.
Trauma to Leg
There is an increased risk of PE in adolescents who
have sustained traumatic injury to their lower limbs.
Anxiety
People with PE feel a sense of impending doom. Signicant oxygen deprivation can contribute to this symptom.
Oral Contraceptives/Estrogen
The estrogen in oral contraceptives causes increased
coagulation of red blood cells, which increases the risk
for PE. In addition, the risk of PE increases with the
combination of smoking and oral contraceptives, especially in women older than age 35.
Medications
A complete medication history can provide clues to a
possible hypercoagulability state. Patients who are taking anticoagulants and are underdosed can be at risk
for PE. Patients taking medication for heart failure,
such as digitalis or angiotensin-converting enzyme
(ACE) inhibitors, are at risk because of chronic heart
failure. Serum estrogen receptor modulators (tamoxifen, raloxifene) increase the risk for PE.
Is the dyspnea related to a preexisting disease?
Key Questions
l
Do you have a history of heart problems, lung prob-
lems (asthma), or anemia?
l
Do you have any numbness or tingling in your body?
Where?
l
Have you noticed any other symptoms?
Past History of Disease
History of coronary artery disease (CAD), heart failure,
valvular heart disease, chronic obstructive pulmonary
disease (COPD), or asthma should raise the level
of suspicion for recurrence or complications of that
disease. Myocardial infarction (MI) can cause sudden
dyspnea in individuals with or without prior history
of CAD. Careful questioning regarding associated
symptoms and risk factors can reveal characteristics of
probable MI (see Chapter 8).
Progressively increasing shortness of breath (SOB)
is frequently a symptom of worsening COPD. It is
often associated with cough that is worse in the morning, clear to yellow color sputum, exercise intolerance,
and fatigue. Chronic progressive dyspnea in the patient
with a history of heart failure or cardiac valve disease
is most frequently a symptom of heart failure. Associated symptoms include peripheral edema, ascites,
cough (possibly with frothy sputum production), chest
pain, and fatigue. Orthopnea (difculty breathing when
lying at) and paroxysmal nocturnal dyspnea (PND)
(a sudden onset of shortness of breath when lying at)
are most often associated with heart failure.
In children with heart disease, dyspnea occurs because of insufcient blood being pumped to the lungs
as a result of congenital structural anomaly or pump
failure or secondary to pulmonary hypertension. Simple
respiratory tract infections can cause severe respiratory insufciency in the child who has cardiopulmonary disease. Associated symptoms include retractions
(including abdominal muscles), tachypnea, nasal aring and grunting, peripheral edema, ascites, cough, and
fatigue.
Chronic progressive dyspnea because of lung involvement can also be present in patients with a history of
systemic illnesses such as sarcoidosis, rheumatological
disease (rheumatoid lungs), cystic brosis, or Goodpasture syndrome (a rare syndrome of progressive glomerulonephritis, hemoptysis, and hemosiderosis); brotic lung
disease such as scleroderma, silicosis, asbestosis; and in
progressive neurological disorders such as myasthenia
gravis, amyotrophic lateral sclerosis (ALS), and multiple
sclerosis.
Periodic recurrent dyspnea is most often the result of
bronchospasm and inamed bronchi caused by asthma.
People with asthma can be relatively symptom free
between episodes and can often identify the cause of
their SOB with little prompting. Symptoms are frequently associated with recent respiratory tract infection, exercise, or exposure to allergens. The patient or
parent may report audible wheezes, decreased exercise
tolerance, and frequent cough. Wheezing is extremely
unusual in the neonatal period and implies intrathoracic
airway obstruction caused by intraluminal obstruction,
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Chapter 14 • Dyspnea
xed airway narrowing, variable narrowing, or external
compression. All of these factors lead to turbulent expiratory ow and audible wheeze.
Hematological diseases can affect the oxygencarrying capacity of the blood, resulting in tissue hypoxia and a decrease in arterial pH, which stimulates
the central nervous system to produce the symptom of
dyspnea. Severe anemia from any cause can result in
this reaction. Dyspnea can occur whenever the oxygencarrying capacity of the blood is decreased because of
the inability of hemoglobin to bind oxygen. Carbon
monoxide poisoning, cyanide poisoning, and methemoglobinemia are examples.
The progressive dyspnea of anemia is usually associated with fatigue, palpitations, light-headedness, or
dizziness.
Hyperventilation
Hyperventilation syndrome, a nonemergent but frightening experience, is usually accompanied by paresthesias around the mouth and of the distal extremities.
Anxiety-related dyspnea should not be diagnosed until
more serious causes have been ruled out.
When dyspnea is caused by pulmonary or cardiac
conditions, the shortness of breath worsens with increasing activity and improves with rest. Dyspnea
caused by anxiety does not improve, and can worsen,
with rest.
What factors precipitate or aggravate the dyspnea?
Key Questions
l
What activities are associated with shortness of
breath?
l
Do you take any medication?
l
Do you have any known allergies (to trees, dust, pol-
len, animals)? Have you been exposed to these recently?
l
Is there anything you can do to help yourself feel less
short of breath, such as sit up, stay indoors, lie down,
or use medication?
Precipitating Factors
Chronic dyspnea of pulmonary origin is most frequently precipitated and aggravated by exposure to
smoke. This is true for both progressive and recurrent
dyspnea. Progressive dyspnea manifested in COPD is
often exacerbated by exertion and is alleviated or improved with rest. As the disease progresses, less and
less intense exercise, even talking, and respiratory
tract infection can result in increased shortness of
breath. Exercise-induced asthma will cause dyspnea
related to activity and is relieved with rest or use of
bronchodilators.
Medication Use
The dyspnea related to asthma may be relieved by use
of bronchodilator agents and steroids.
Allergies
Exposure to cold and/or allergens, exercise, and viral
respiratory tract infections frequently precipitate chronic
recurrent dyspnea associated with asthma.
Recumbence, missed medications, high sodium intake, and exertion often precipitate chronic dyspnea
associated with heart failure. This applies to both progressive and recurrent chronic dyspnea.
Alleviating Factors
Alleviating factors for dyspnea include sitting upright,
taking diuretic medications, using bronchodilators, and
resting for a prolonged period.
Is the dyspnea caused by a neuromuscular problem?
Key Questions
l
Are your immunizations up to date?
l
If a child: Has the child eaten any honey?
l
Do you live on a farm?
l
If a child: Is the child at risk for lead poisoning?
l
Do you have a headache, muscle weakness, or other
symptoms?
Immunizations
Lack of childhood or adult immunizations for poliomyelitis or tetanus can lead to paralysis or tetany of the
respiratory musculature, resulting in dyspnea and subsequent respiratory distress.
Honey
Honey is a common source of contamination of Clostridium botulinum, which can cause respiratory distress
in infants and small children. The incubation period is
only a few hours. Nausea, vomiting, and diarrhea result,
followed by cranial nerve involvement, diplopia, weak
suck, facial weakness, and absent gag reex. Generalized hypotonia and weakness then develop and can
progress to respiratory failure.
Farm Residence
Organophosphate chemicals that are commonly used
as insecticides can cause a myasthenia-like syndrome
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163
in children exposed to these toxins. Children residing
on farms are most at risk.
Neuromuscular Effects
Abnormalities of neural or neuromuscular transmission
to the respiratory muscles can result in paresis or paralysis, leading to alveolar hypoventilation. Direct involvement of the respiratory muscles affected by systemic
musculoskeletal diseases can lead to a reduction of vital
capacity and total lung capacity and result in hypercapnic hypoventilation and dyspnea. Examples of neuromuscular health problems leading to dyspnea include
infections, such as poliomyelitis, tetanus, and central
nervous system insult such as ALS. Urge incontinence
can be an early sign of multiple sclerosis; easy fatigability can be associated with myasthenia gravis.
In children, some causes that affect the primary respiratory center are myopathies, insecticide poisoning,
and lead poisoning.
Secondary Causes
Diseases that affect the central nervous system and
produce respiratory distress include meningoencephalitis, seizures, and central nervous system lesions.
Does the patient have any pertinent risk factors that will
point me in the right direction?
Key Questions
l
Do you smoke? Have you ever smoked? Are you
regularly exposed to cigarette smoke?
l
What type of work do you do?
l
Have you had a recent weight gain?
l
Have you ever had eczema?
Risk Factors
Individuals at risk for developing dyspnea are those
with a history of pulmonary and/or heart disease, cigarette smokers and those subjected to passive exposure
or second-hand smoke, people exposed to noxious
environmental pollutants, and individuals with a predisposition to allergies or asthma.
active and nonobese counterparts. Obese people may
report dyspnea, especially during exercise. This is
caused by an increase in the metabolic requirement for
a given amount of work. In addition, the diaphragm
moves against increased abdominal pressure and the
chest wall is heavier, resulting in more energy required
to maintain ventilation.
Eczema History
Asthma occurs in 20% to 40% of children with a history
of atopic dermatitis.
DIAGNOSTIC REASONING: FOCUSED
PHYSICAL EXAMINATION
Note General Appearance and Observe Posture
Patients who appear in acute distress with manifestations of severe oxygen deprivation require emergent
evaluation and treatment. Assess vital signs immediately. Tachypnea and hypopnea are critical clues to
impending respiratory failure. Use of accessory muscles to breathe, posturing, and chest retraction all
point to severe dyspnea. The severity of the dyspnea
almost always correlates with the severity of the
problem. In such situations consider pulmonary embolism, anaphylaxis, foreign body aspiration, pneumothorax, status asthmaticus, and severe heart failure. Patients presenting with symptoms of COPD,
anemia, mild asthma, and mild heart failure appear
less acutely ill.
Determine if the patient has to lean forward or sit
up to breathe comfortably. With severe respiratory
distress or upper airway obstruction, an infant can
adopt a posture of hyperextension of the trunk and
neck. A child with epiglottitis prefers to sit up and
lean forward.
A child who is in acute respiratory distress, sitting
forward, and perhaps speaking with a mufed voice or
drooling may have epiglottitis and immediate assistance should be secured. Do not attempt to lay the child
down or inspect the throat because this can occlude the
airway.
Work
Occupational exposure to asbestos, silicon, paint and
chemical fumes, and coal dust place the patient at risk
for lung disease with resultant dyspnea.
Obesity
Physically deconditioned and obese people report dyspnea on exertion more frequently than their physically
Assess Level of Consciousness
Diminished level of consciousness, confusion, and
restlessness are manifestations of hypoxia in a patient
experiencing respiratory problems. Frequently the patient with a PE expresses a sense of impending doom.
An acutely ill child can have an alteration in level of
consciousness, restlessness, mouth breathing, and aring of the nostrils.
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Observe Chest Movement
Place the patient in a sitting or side-lying position with
the chest exposed. The chest cannot be adequately
viewed through clothing. Many respiratory abnormalities are unilateral or localized. Compare ndings on
one side of the body with those on the other. Also compare front to back. Pneumothorax and PE can cause
unequal expansion of the chest.
Inspect the Shape and Symmetry of the Chest
Cardinal features of restrictive pulmonary disease are
deformities of the chest wall and reduction in lung volume and pulmonary compliance secondary to pathological changes in the lung parenchyma or pleura. Examples
of deformities that cause decreased lung volume include
kyphosis, scoliosis, and kyphoscoliosis. Decreased volume necessitates an increase in respiratory rate to maintain a normal volume. The work of breathing must be
increased to overcome the reduced compliance.
Kyphoscoliosis is associated with marked structural
abnormality of the thoracic cage, leading to abnormal
positioning and functioning of the respiratory muscles.
The lungs are compressed by the thoracic deformity,
leading to a small lung volume. Breathing entails a
high work and energy cost, and dyspnea can appear.
An increased anteroposterior (AP) diameter indicates air trapping. This is a frequent nding in individuals with COPD. Other musculoskeletal chest abnormalities to note include pectus excavatum and
pectus carinatum. These conditions can contribute to
chest infection and respiratory failure because of decreased lung volume and ability to cough. Bronchomalacia, a softening of the bronchial tissue, is an abnormality associated with pectus excavatum. Pectus
carinatum is associated with chronic lung disease such
as asthma or with cystic brosis, heart disease such as
mitral valve prolapse, Marfan syndrome, and idiopathic scoliosis. Harrison sulci are exaggerated grooves
running parallel to the subcostal margins, produced by
prolonged diaphragmatic traction, and are associated
with chronic airway disease or rickets.
In the presence of neuromuscular disease, chest
movement in children should be examined in both the
supine and sitting positions. Diaphragmatic weakness
leads to paradoxical abdominal movements in the supine
position, which can be missed if the child is examined
only in the sitting position.
Respiratory distress triggered by placing the child
in the supine position can be the only subtle abnormality in older children with mediastinal compression of
the trachea.
Look for Retractions
In normal breathing, inspiration is the work necessary
to overcome the elastic forces of the lung, the tissue
viscosity of the lung and chest wall, and airway resistance. When there is a problem with any of these, the
accessory muscles (sternocleidomastoid, serratus anterior, and external intercostal) are recruited. Contraction
of these muscles causes forceful expansion of the thorax, resulting in increased negative pressure that draws
in the soft tissues of the chest wall and results in retractions. Retractions begin in lower intercostal spaces and
then move up to the higher spaces. In an infant, head
bobbing in time with respiration reects use of the
accessory muscles of respiration.
Observe the Rate, Rhythm, and Depth
of Respiration for 1 Full Minute
In children, the respiratory rate should be counted
while the child sleeps, if possible.
Tachypnea is an early sign of most pulmonary, parenchymal, cardiac, or systemic causes of respiratory
distress. Hyperventilation can occur secondary to acidosis or central nervous system disease. Central nervous system depression can lead to hypoxemia and
shock; systemic infection can lead to metabolic acidosis and trigger hyperventilation.
Exhaling should take about twice as long as inhaling, but in patients with COPD, it can take up to four
times longer. Rhythm should be even, with occasional
sighs. Shallow respirations, which are rapid, indicate
that restrictive forces must be overcome. Box 14-1
describes abnormal breathing patterns.
Box 14-1
Cheyne-Stokes respirations are manifested by rhythmic
increase and decrease in depth, punctuated by regular episodes of apnea. This can be a sign of severe heart failure,
or neurological disease.
Tachypnea is rapid breathing with no change in depth,
and can be ca used by hypoxia, pain, fever, or anxiety.
Consider pulmonary embolism, foreign body aspi ration,
anaphylaxis, pneumothorax, heart failure, asthma, or
pneumonia.
Asymmetrical chest movement with respirations can be
observed in lobar pneumonia, pleural effusion, or any condition that affects just one side of the chest.
Use of accessory muscles indicates respiratory distress.
Observe for bulging or retraction of the intercostal, sternocleidomastoid, and/or trapezius muscles. Nasal flaring is an
objective manifestation of hypoxia.
Abnormal Breathing Patterns
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Listen for Stridor
Stridor is caused by extrathoracic, inspiratory, dynamic
narrowing of the airway in the oropharynx, glottis,
subglottic region, or midtrachea. Any condition that
causes further decrease in the lumen of the airway will
obstruct airow and produce stridor. Inspiratory stridor
usually indicates a supraglottic obstruction. If the obstruction varies or is extrathoracic (above the vocal
cords), inspiration is affected more because the negative intra-airway pressure during inspiration tends to
collapse the extrathoracic airway. If the obstruction
varies and affects the intrathoracic airways, expiration
is prolonged because the positive intrathoracic pressure tends to collapse these airways during expiration.
Expiratory or biphasic respiratory stridor generally indicates an obstruction at or below the larynx.
With severe narrowing of the air passage, stridor
can be audible on both inspiration and expiration, but
is worse during inspiration. Biphasic or expiratory
stridor alone usually indicates a more signicant obstruction. Supraglottic stridor is usually quiet and wet,
and is associated with a mufed voice, dysarthria, and
a preference to sit. Subglottic lesions produce a loud
stridor, often causing a hoarse voice, barky cough, and
possibly facial edema. Inspiratory stridor can be a sign
of incomplete obstruction of the airway by a foreign
body.
Infants younger than 6 months who present with
stridor can have an underlying anatomical abnormality that may be symptomatic secondary to an acute
illness. Common anomalies that predispose the infant
to upper airway obstruction are anomalous vascular
rings, laryngeal webs, laryngomalacia, or tracheomalacia. Stridor in older children can indicate foreign
body aspiration, infection, inammation, trauma, or
tumor.
Listen for Audible Wheeze
Expiratory wheezing is a high-pitched musical sound
caused by partial airway obstruction. It is commonly
associated with disorders of the lower respiratory tract
that cause inammation, infection, or bronchoconstriction such as asthma and bronchitis.
Increased inspiratory effort suggests disease in the
upper airways, whereas increased expiratory effort
suggests disease in the smaller airways or lower respiratory tract.
Listen for Voice Changes
Voice changes can occur in association with upper
airway obstruction. Paralysis of the vocal cords results
in dysphonia. Subglottic stenosis results in decreased
volume of the voice because a much smaller column
of air is making the vocal cords vibrate. Involvement
of the supraglottic area, proximal to the vocal cords,
can result in hyponasality or mufed voice such as in
tonsillitis and epiglottitis. A normal voice with stridor can indicate a subglottic or tracheal lesion (see
Chapter 21).
Take Pulse, Temperature, and Blood Pressure
Palpate the radial, femoral, popliteal, and pedal pulses
for rate and quality.
Tachycardia increases cardiac output. It occurs
either as a result of primary heart disease or as a
secondary process in response to oxygen deprivation
because of PE, pneumonia, fever, and/or heart failure.
Tachycardia and drowsiness can indicate metabolic
acidosis. Bradycardia is usually seen late in respiratory disease.
Tachycardia can occur with an irregular pulse, signaling heart failure from atrial brillation, and/or heart
block. Diminished peripheral pulses indicate possible
atherosclerotic vessel disease or decreased cardiac
output.
Fever can indicate epiglottitis or any other upper
and/or lower respiratory tract infection.
Orthostatic hypotension can be secondary to dehydration associated with pneumonia or status asthmaticus. Anaphylaxis is also manifested by severe hypotension. Pulsus paradoxus, an inspiratory drop in systolic
blood pressure of more than 10 mm Hg, is caused by
greater inspiratory effort from increased airway resistance. Negative intrathoracic pressure is associated
with increased afterload and low systolic blood pressure. In heart failure, decreased stroke volume reduces
the systolic blood pressure. Compensatory vasoconstriction maintains a constant diastolic pressure and,
along with the decreased systolic pressure, can produce
a decreased pulse pressure.
Inspect the Oral Cavity
First observe the oropharyngeal cavity for any evidence of a foreign body obstructing the airway. Evidence of vomitus can indicate possible aspiration. Note
the color of the tongue and mucous membranes for
signs of central cyanosis.
Inspect the posterior pharynx for peritonsillar cellulitis, retropharyngeal abscess, or other intraoral pathology that might be causing obstruction. Lift the
jaw forward. Obstruction of the airway associated
with micrognathia, depressed airway reexes, or an
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enlarged tongue, will diminish with this maneuver
because the tongue will be lifted off the posterior pharynx. If epiglottitis is suspected, do not examine the oral
cavity.
Inspect the Nose
Assess the patency of the nares. Fifty percent of airway
resistance comes from the nose. Check for nasal aring.
An infant who has nasal aring is using a compensatory
mechanism to decrease airway resistance. Noisy, difcult breathing in an infant, especially while feeding, can
signal choanal atresia. A deviated septum compromises
the patency of one side of the nose when there is mucosal swelling.
Palpate the Neck
Neck masses caused by intraoral, paratracheal, or
intrathoracic malignant disease can cause respiratory distress. Inspect the position of the trachea. To
assess the trachea for lateral displacement, position
your index nger rst on the right side of the suprasternal notch and then on the left. If the trachea has
shifted to the side, you will feel the wall on one side
but only soft tissue on the other. This is most likely
to occur with pneumothorax. Observe the neck for
jugular venous distention; this is a sign of heart
failure.
Examine the Skin and Extremities
Note cyanosis. Bluish color seen in the lips and
mucous membranes of the mouth (central cyanosis)
is associated with low arterial saturation and can
result from inadequate gas exchange in the lungs
or from cardiac shunting. Cyanosis implies more
than 5 g/100 mL of desaturated hemoglobin, but its
absence does not imply that hypoxemia is not present. Dark-skinned patients’ mucous membranes
can appear gray with central cyanosis. Central cyanosis can also be seen in people with COPD. Bluish
color of the extremities (peripheral cyanosis) may
be observed in white individuals and is associated
with low venous saturation, resulting from vasoconstriction, vascular occlusion, or reduced cardiac
output.
Pallor of sclera or nail beds can be a manifestation
of severe anemia.
Note clubbing, which is characterized by the loss of
the angle between the skin and nail bed. Clubbing is a
manifestation of chronic tissue hypoxia that occurs with
lung cancer and other chronic lung diseases but can also
be idiopathic. It is uncommon in children other than
those with cystic brosis, cyanotic congenital heart
disease, thyrotoxicosis, and in celiac disease. Clubbing
develops rapidly with infective endocarditis.
Test for peripheral edema. Edema of the lower extremities can be a sign of increased right-heart lling
pressure caused by primary lung disease or leftventricular failure. Make note of how high the edema
extends up the extremity. In children, the location of
peripheral edema is age dependent. In young infants,
edema occurs as hepatomegaly and periorbital or ank
edema. In older children, lower extremity edema can
occur.
Note any angioedema. The presence of generalized
or local urticaria is objective evidence of probable
anaphylaxis.
Check skin perfusion by pressing on the skin of
a nger or sole of a foot and saying “capillary rell”
after removing the pressure. In a normal nding, the
color returns to the skin in 2 seconds or before you can
nish saying the words.
Feel the skin for diaphoresis. When respiratory
muscles are working at their maximum level to overcome increased resistive and elastic forces, the child
will sweat, especially on the forehead and above
the lip.
Palpate the Chest
Using the palmar surface of the hands, palpate the entire chest for tenderness, depressions, bulges, and
crepitus (presence of air in the subcutaneous tissues).
Crepitus can indicate a chest injury, pneumothorax, or
cutaneous emphysema.
Pneumothorax, atelectasis, pneumonia, and partial
paralysis of the diaphragm will result in reduced expansion of one side of the chest wall, and chest wall
motion will be decreased.
Assess for Tactile Fremitus
Fremitus is diminished in pneumothorax, asthma, emphysema, and other conditions that trap air in the lung.
Tactile fremitus intensity can be increased in pneumonia, heart failure, and tumor, all conditions that increase
the lung density.
Percuss the Chest
Sounds produced by percussion indicate the density of
lung tissue (see Chapter 11). In children, transmission of
a percussion note and assessment of the quality of transmitted sound are useful to reveal an area of consolidation or effusion that would be difcult to auscultate with
an uncooperative child.
Chapter 14 • Dyspnea
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167
EVIDENCE-BASED PRACTICE
A systematic review was conducted to review the evidence
regarding the accuracy of the physical examination in assessing the thorax for pleural effusion. Eight physical examination
techniques were evaluated: manual percussion; auscultatory
percussion (tapping on the manubrium and listening to
the posterior chest with a stethoscope simultaneously) for
decreased resonance; auscultation for breath sounds, crackles, and pleural friction rubs; chest expansion; tactile vocal
Reference: Wong CL, Holroyd-Leduc J, Straus SE: Does this patient have a pleural effusion? JAMA 301:309-317, 2009.
Auscultate Breath Sounds
Auscultation of bronchial or bronchovesicular breath
sounds over the peripheral lungs can indicate consolidation, which occurs when lungs ll with exudate.
Young children normally have bronchovesicular sounds
because of the thinness of their chest wall.
If breath sounds are diminished over all lung elds,
suspect shallow breathing, lack of air movement, neuromuscular diseases, obesity, or COPD. Breath sounds
will be inaudible in areas of pneumothorax.
Abnormal lung sounds are superimposed on normal
sounds and can be auscultated over any area of the lung
eld during inspiration or expiration. Documentation of
abnormal lung sounds should include type of sound,
location where it is heard, and the phase(s) of respiration
in which it is noted. In small children it can be difcult
to distinguish upper and lower airway sounds. Listening
with the stethoscope over the nose or mouth, and then
returning to the lungs, can help to identify the ndings.
Crackles or rales are discontinuous popping sounds
heard most often during inspiration. They are caused by
the explosive equalization of gas pressure between two
compartments of the lung when a closed section of the
airway that separates them suddenly opens. They indicate the presence of uid, mucus, or pus in the smaller
airways. Fine crackles are soft and high pitched. Medium
crackles are louder and lower pitched. Coarse crackles
are moist and more explosive.
The frequency and timing of crackles are the important parts of assessment. In resolving pneumonia, crackling is heard on inspiration caused by a mix between the
aerated and nonaerated alveoli and bronchioles. In airways that are swollen and narrowed, such as in asthma
or bronchiolitis, generalized medium or coarse crackles
Physical Examination Techniques to Detect Pleural Effusion
fremitus; and vocal resonance. Dullness to manual percussion incre ased the likelihood of pleural effusion. However, a
chest x-ray is necessary to confirm a diagnosi s. If tactile
fremitus is not decreased in a patient at low risk for pleural
effusion, a chest x -ray may not be necessary. In summary,
dullness to percussion and tactile fremitus are the most useful findings when evaluating a patient for pleural effusion.
Wheezing is frequently described as a whistling
sound and may be heard during inspiration, expiration,
or both. The sound is high pitched and musical. Wheezing indicates that there is uid in the large airways such
as in severe heart failure or, more often, heralds bronchospasm, as seen in asthma. In addition, localized
wheezing can accompany incomplete obstruction of the
airway by a foreign body.
A wheeze of xed pitch occurring with inspiration and
expiration suggests a localized abnormality. Wheezes of
varying pitch occurring predominantly throughout expiration reect the narrowing of airways of different calibers.
Rhonchi are continuous, deep-pitched, coarse breath
sounds usually heard during expiration. Rhonchi are
frequently present when the patient has bronchitis or
pneumonia.
Pleural friction rub is a grating or squeaking sound
usually heard in the lateral lung elds during inspiration
and expiration. It indicates that parietal and visceral
pleural linings are inamed and are rubbing together as
can occur with pneumonia, pleural effusion, pleuritis,
and tumors. It is often accompanied by limited chest
expansion because of pain.
If abnormal lung sounds are detected, additional
auscultation for bronchophony, egophony, and whispered pectoriloquy is indicated. Consolidation will
produce abnormal ndings for each of these tests. To
test for bronchophony, instruct the patient to say
“ninety-nine.” The words are heard louder and clearer
than usual. In egophony, instruct the patient to say
“ee.” This sound is transmitted as “ay” if consolidation
is present. To test whispered pectoriloquy, instruct the
patient to whisper a sentence. Whispered sounds are
louder and clearer than normal.
are heard throughout both phases of respiration. Early
inspiratory crackles are heard in COPD. Mid to late inspiratory crackles are more likely a sign of interstitial
lung disease or heart failure. Crackles can be heard over
the site of a pulmonary embolus.
Auscultate Heart Sounds
In COPD, lung hyperination can mufe heart sounds.
Poor tissue oxygenation can result in tachycardia. In
children, mufed heart sounds can indicate pericarditis.
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Chapter 14 • Dyspnea
In heart failure, the rst and second heart sounds
(S1 and S2) can equal the peripheral pulse rate. If the
peripheral pulse rate is less than the heart rate, this
pulse decit is a sign of decreased cardiac output. S3
(ventricular gallop) is an early sign of heart failure and
is heard best at the apex of the heart. S4 (atrial gallop)
in children typically indicates a stressed heart and heart
failure. In adults it can be the result of hypertension,
MI, or CAD causing heart failure. A summation gallop
can also occur with heart failure; this is the result of
S3, S4, and rapid rate.
Listen for the presence of any murmurs and note their
location, grade of loudness, timing, or radiation. Incompetent heart valves can be the cause of heart failure.
LABORATORY AND DIAGNOSTIC STUDIES
Diagnostic tests are indicated in almost all initial
evaluations of the patient presenting with shortness of
breath (SOB). Posteroanterior (PA) and lateral chest
radiographs, hemoglobin level and spirometry are useful preliminary tests.
Transcutaneous Pulse Oximetry
Oximetry measures the fraction of oxygen carried in
hemoglobin and provides noninvasive information
about the delivery of oxygen from the atmosphere to
the pulmonary capillaries. The partial pressure of oxygen in arterial blood (PaO2) in healthy adults ranges
from 80 to 103 mm Hg, and more than 95% saturation
of hemoglobin is considered normal. In children, a
pulse oximetry reading of 95% to 98% is normal, 90%
to 95% is mild hypoxia, 85% to 90% is moderate hypoxemia, and less than 85% is severe hypoxemia.
Chest Radiography
Chest radiographs are essential in the diagnosis of dyspnea and can show pneumothorax, pneumonia, malignant disease, pleural disease, foreign body, or pulmonary edema. They can also provide clues to other causes
of dyspnea such as cardiomegaly, deformities of the
chest bones and musculature, and the position of the
diaphragm. When a foreign body is suspected, both inspiratory and expiratory chest x-rays can be helpful.
Electrocardiography
An electrocardiogram (ECG) can provide important
information about myocardial ischemia, arrhythmias,
pericarditis, or the presence of pulmonary disease. Cardiopulmonary exercise testing can be done if the severity
of the dyspnea is disproportionate to objective tests, there
are coexisting cardiac and pulmonary causes, or if deconditioning, obesity, or psychological factors are suspected.
Echocardiography
An echocardiogram is performed when cardiac disease
is suspected; this test can dene the cause of dyspnea
related to heart chamber size, valves, pericardial disease,
and ventricular function.
Hemoglobin and Hematocrit
Signicantly decreased hemoglobin and hematocrit
levels suggest anemia as a possible cause of dyspnea.
Erythrocytosis can indicate chronic hypoxia resulting
from a number of causes including COPD, carbon
monoxide (CO) poisoning, and smoking.
Spirometry
Spirometry is indicated if the dyspnea is related to obstructive or restrictive lung disease. Spirometry measures
forced vital capacity (FVC), 1-second forced expiratory
volume (FEV1), the FEV1/FVC ratio, and the peak expiratory ow rate (PEFR). In obstructive lung disease (i.e.,
asthma and COPD), the FEV1 and the FEV1/FVC ratio
are less than predicted. In restrictive lung disease (i.e.,
pneumonia, pneumothorax, pleural effusion), the FVC is
reduced and the ratio is normal or elevated. Spirometry
that indicates restrictive disease or mixed obstructive restrictive disease should have follow-up studies to test for
lung volumes with either helium dilution, body plethysmography, and/or a diffusion capacity.
Additional Testing
Additional diagnostic tests may be indicated after the
initial data gathering and can include the following:
l
Computed tomography (CT) provides more detailed
assessment of mass lesions.
l
Computed tomography pulmonary angiography
(CPTA) conrms PE.
l
A D-dimer assay can help diagnose thrombosis. Nor-
mal ndings rule out thrombosis; abnormal ndings
may indicate thrombosis but do not rule out other
potential causes. It is used to exclude thromboembolic disease where the probability is low.
l
Wells criteria can be applied to arrive at a score to
estimate the probability of pulmonary embolism.
l
Complete blood count with differential is used to
determine the presence of bacterial infection.
l
Blood urea nitrogen and creatinine levels help assess
renal function. Renal insufciency frequently presents with dyspnea as a result of the combined effects
of volume overload and anemia.
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