Respiratory Distress Patient Tintinalli 7th Ed

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Tintinalli's Emergency Medicine > Section 8. Pulmonary Emergencies > Chapter 65. Respiratory Distress >
RESPIRATORY DISTRESS
Common respiratory symptoms that bring patients to the ED include dyspnea (sometimes with the associated findings of
hypoxia and hypercapnia), wheezing, and cough. Hiccups are an infrequent presenting symptom, but when persistent,
they are very distressing to the patient. Cyanosis can be associated with pulmonary, vascular, and hematologic
conditions. Pleural effusion can be caused by a variety of pulmonary and cardiac diseases. This chapter discusses these
symptoms, signs, and disorders as they relate to evaluation of emergency patients. Despite the increasing availability of
and reliance on ancillary tests, the assessment of patients still begins with an accurate history and a careful physical
examination to make the wisest use of ancillary tests. 1

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DYSPNEA
Dyspnea is a subjective feeling of difficult, labored, or uncomfortable breathing, which patients often describe as
"shortness of breath," "breathlessness," or "not getting enough air." Dyspnea does not result from a single
pathophysiologic mechanism, but approximately two thirds of symptomatic patients presenting to the ED have a cardiac or
a pulmonary disorder.
Dyspnea is frequently associated with other respiratory symptoms. Tachypnea is rapid breathing; it may or may not be
associated with dyspnea. Orthopnea is dyspnea in the recumbent position. It is most often the result of left ventricular
failure, but can also be seen with diaphragmatic paralysis or chronic obstructive pulmonary disease (COPD). Paroxysmal
nocturnal dyspnea is orthopnea that awakens the patient from sleep. Trepopnea is dyspnea associated with only one
of several recumbent positions. Trepopnea can occur with unilateral diaphragmatic paralysis, with ball-valve airway
obstruction, or after surgical pneumonectomy. Platypnea is the opposite of orthopnea: dyspnea in the upright position.
Platypnea results from the loss of abdominal wall muscular tone and, in rare cases, from right-to-left intracardiac
shunting, as occurs from a patent foramen ovale. Hyperpnea is essentially hyperventilation and is defined as minute
ventilation in excess of metabolic demand. Hyperpnea may not be associated with dyspnea, and dyspnea is not always
associated with increased minute ventilation.
Pathophysiology
Dyspnea is a complex sensation that involves both objective and subjective elements. Dyspnea has no defined neural
pathway, and the perceived difficulty probably arises from the interaction of several pathophysiologic mechanisms. 2 Input
from any or all of the following receptors is integrated in a complex manner in the central nervous system (CNS) at both
the subcortical and cortical levels:
A conscious sense of the voluntary peripheral skeletal and respiratory muscular effort that occurs with
increased work of breathing
Stimulation of upper airway mechanical and thermal receptors
Decreased stimulation of chest wall afferents
Stimulation of central hypercapnic chemoreceptors in the central medulla
Stimulation of peripheral hypoxic chemoreceptors, primarily in the carotid body in concert with those in the
aortic arch
Stimulation of a variety of lung receptors, including intraparenchymal pulmonary stretch receptors, airway
irritant receptors, and unmyelinated receptors that respond to interstitial edema or a change in compliance
Stimulation of peripheral vascular receptors, including the right atrial and left atrial mechanoreceptor and the
pulmonary artery baroreceptor
Many authors believe that dyspnea results from afferent mismatch, when feedback from these peripheral receptors
indicates that the work of breathing is greater than would be expected by the patient's level of activity. 3
Clinical Features
The causes of dyspnea can be divided into general categories (Table 65-1). The presence or degree of dyspnea is
difficult to measure, although categorical scales (e.g., the Borg or Fletcher scales) and visual analog scales can be used to

gauge response to therapy.4 In an effort to identify imminent respiratory failure, the physician should specifically evaluate
for tachypnea, tachycardia, stridor, and use of the accessory respiratory muscles, including the sternocleidomastoid,
sternoclavicular, and intercostals. Other signs and symptoms of imminent respiratory failure are inability to speak as a
consequence of the breathlessness, agitation or lethargy as a consequence of hypoxia, depressed consciousness due to
hypercapnia, and paradoxical abdominal wall movement (abdominal wall retracts inward with inspiration, indicating
diaphragmatic fatigue). In patients with any of these signs or symptoms, oxygen should be administered and the need for
airway control and mechanical ventilation anticipated. Lesser degrees of dyspnea allow for a more detailed medical
history, physical examination, and indicated ancillary tests.
Table 65-1 Differential Diagnosis of Consequence: Dyspnea
Most Common Causes Most Immediately Life-Threatening
Obstructive airway disease: asthma, chronic obstructive Upper airway obstruction: foreign body, angioedema,
pulmonary disease hemorrhage
Heart failure/cardiogenic pulmonary edema Tension pneumothorax
Ischemic heart disease: unstable angina and myocardial Pulmonary embolism

infarction
Pneumonia Neuromuscular weakness: myasthenia gravis, Guillain-Barr
syndrome, botulism
Psychogenic Fat embolism
Diagnosis
A detailed medical history often identifies the primary process resulting in dyspnea. Patients with underlying chronic
disorders can frequently specifically and accurately self-diagnose their exacerbations. The medical history should include
recent infectious and environmental exposures that may impair respiratory function. Patients who require daily
medications for symptom control should be questioned carefully about compliance and possible drug interactions.
DIFFERENTIATING CARDIAC FROM PULMONARY CAUSES OF DYSPNEA

Differentiating between cardiac and pulmonary causes of dyspnea is one of the most important, and frequently most
difficult tasks, an emergency physician faces. The treatment and prognosis differs vastly, and embarking down the wrong
pathway of treatment can have significant adverse consequences. 5 Several factors have been found to assist in this
decision-making process, although few of them are definitive by themselves (Table 65-2).6
Table 65-2 Factors Supporting Heart Failure as the Cause of Dyspnea
Finding LR + (95% CI) LR (95% CI)
Clinical gestalt 4.4 (1.810.0) 0.45 (0.280.73)
History
Heart failure 5.8 (4.18.0) 0.45 (0.380.53)
Myocardial infarction 3.1 (2.04.9) 0.69 (0.580.82)
Coronary artery disease 1.8 (1.12.8) 0.68 (0.480.96)
Symptoms
Paroxysmal nocturnal dyspnea 2.6 (1.54.5) 0.70 (0.540.91)
Orthopnea 2.2 (1.23.9) 0.65 (0.450.92)
Edema 2.1 (0.925.00) 0.64 (0.391.10)

Dyspnea on exertion 1.3 (1.21.4) 0.48 (0.350.67)
Physical exam
S 3 gallop 11.0 (4.925.0) 0.88 (0.830.94)
Jugular venous distention 5.1 (3.27.9) 0.66 (0.570.77)
Hepatojugular reflex 6.4 (0.8151.00) 0.79 (0.621.00)
S4 1.6 (0.475.50) 0.98 (0.931.00)
Wheezing 0.52 (0.380.71) 1.3 (1.11.7)
Chest x-ray
Pulmonary venous congestion 12.0 (6.821.0) 0.48 (0.280.83)
Interstitial edema 12.0 (5.227.0) 0.68 (0.540.85)
Alveolar edema 6.0 (2.216.0) 0.95 (0.930.94)
Cardiomegaly 3.3 (2.44.7) 0.33 (0.230.48)
ECG
Atrial fibrillation 3.8 (1.78.8) 0.79 (0.650.96)
Any abnormal finding 2.2 (1.63.1) 0.64 (0.470.88)
B-type natriuretic peptide <80 picograms/mL 0.06 (0.030.13) 3.3 (1.86.3)
The finding of an S 3 gallop on physical examination, or pulmonary venous congestion or interstitial edema on chest x-ray
all strongly suggest congestive heart failure (CHF) as the cause of the dyspnea (Figure 65-1).6 The physician's overall
gestalt of the diagnosis, the presence of jugular venous distension on examination, and alveolar edema on chest x-ray
suggest CHF. The presence of wheezing, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and leg edema
are not useful in discriminating between cardiac and pulmonary causes. Conversely, the absence of these findings does
not exclude CHF. Only a B-type natriuretic peptide (BNP) <80 picograms/mL is useful in ruling out a cardiac cause.6 In a
study of 417 patients with a history of COPD or asthma, a high clinical suspicion for CHF, an S 3 gallop, and edema on
chest x-ray suggested CHF as the cause of the dyspnea. 7 Finally, echocardiography, when available, can be helpful in
determining the cause.
Figure 65-1.

Pulmonary edema. Cardiomegaly is present, the pulmonary vasculature is engorged, and cephalization of flow is present.
LABORATORY/RADIOGRAPHIC EVALUATION
A number of ancillary tests aid in determining the severity and specific cause of dyspnea. Pulse oximetry is a rapid but
insensitive screening test for disorders of gas exchange, and results may be normal in acute dyspnea. Arterial blood gas
(ABG) analysis is more sensitive for detecting impaired gas exchange, but results may also be normal in acute dyspnea,
and ABG analysis cannot evaluate the work of breathing. Rarely, patients who appear dyspneic or tachypneic but who
exhibit no evidence of hypoxia or pulmonary disease are shown to be hyperventilating from metabolic acidosis on ABG
testing. A chest radiograph may indicate the general category of primary disease: infiltrate, effusion, and pneumothorax.
Bedside spirometric analysis [peak expiratory flow (PEF)] before and after bronchodilator therapy can be used to diagnose
and treat dyspnea resulting from asthma or COPD, although it requires voluntary effort that might be difficult for dyspneic
patients. Other potentially useful tests include an ECG and determination of hemoglobin (Hb) level. Uncommonly, the
cause of dyspnea cannot be identified by the history, the physical examination, or these ancillary tests, and specialized
testing, including cardiac stress testing, echocardiography, formal pulmonary function testing, CT scanning of the chest, or
combined cardiopulmonary exercise testing, is indicated.
B-Type Natriuretic Peptide

BNP is a 32-amino acid polypeptide secreted by ventricular myocytes in response to volume expansion and pressure
overload. Assays exist that measure BNP or its precursor, N-terminal pro-BNP. Two methods of assay exist, an enzyme-
linked immunosorbent assay (ELISA) and a radioimmunoassay. For the measurement of BNP, the ELISA is more accurate
than the radioimmunoassay.8
In the patient with CHF and volume overload, BNP elevates because of the stretching of the cardiac muscle. BNP values
should be normal in noncardiac causes of dyspnea. A BNP that is very low, <100 picograms/mL, has a LR of 0.14 or
lower, 6,7,9,10 and a cutoff of <80 picograms/mL is associated with a LR of 0.06 or lower, 6,10,11 making very low levels
useful for excluding the diagnosis of CHF in low and moderate pretest probability patients. A very high level, >400
picograms/mL, is moderately useful for establishing the diagnosis of CHF, with a LR + of 5.11 Values between 100
picograms/mL and 400 picograms/mL are not helpful because many other diseases can cause mild elevations of BNP. This

said, combining BNP with clinical judgment may increase diagnostic accuracy, 9 and may reduce hospitalization rates and
length of stay.12
Treatment
Just as there is no single cause of dyspnea, there is no single treatment. In severe dyspnea, the primary treatment goal is
maintenance of the airway and oxygenation with a Pa O2 >60 mm Hg and/or arterial oxygen saturation (SaO2 ) 90%.
After this is ensured, or for patients with lesser degrees of dyspnea, disorder-specific treatment can be provided. Patients
with unrelieved dyspnea at rest, particularly those with terminal malignancies, may benefit from opioids or
benzodiazepines. 13


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HYPOXEMIA
Hypoxia is insufficient delivery of oxygen to the tissues. The amount of oxygen available to the tissues is a function of
the arterial oxygen content (Ca O2 ) and blood flow (Formula 65-1).
Formula 65-1
Formula for calculating tissue oxygenation.
Tissue hypoxia occurs in states of low cardiac output, low Hb concentration, or low Sa O2 . The percent oxygen saturation
of arterial Hb is, in turn, dependent on the Pa O2 , as described by the oxygen-Hb dissociation curve. Hypoxemia is an
abnormally low arterial oxygen tension. Under most situations, hypoxemia is the most common cause of hypoxia.
Although the terms hypoxia and hypoxemia are generally used interchangeably, one can occur without the other. For
example, in states of low Pa O2 (hypoxemia) with concomitant polycythemia, the patient may have no tissue hypoxia.
Alternatively, severely anemic patients may suffer tissue hypoxia despite a normal Pa O2 . Hypoxemia is arbitrarily defined
as a Pa O2 <60 mm Hg. As noted above, patients with hypoxemia may not necessarily have dyspnea, and patients with
dyspnea may not have hypoxemia.
Relative hypoxemia is the term used when the arterial oxygen tension is lower than expected for a given level of inhaled
oxygen. The degree of relative hypoxemia can be assessed by calculating the alveolar arterial ( A-a) oxygen partial
pressure gradient, [P( A-a)O2 ]. The A-a oxygen ( A-a O2 ) gradient measures efficiency of oxygen transfer from the lungs to
the circulation. Alveolar oxygen partial pressure is determined by the inhaled oxygen concentration (21% for room air),
atmospheric pressure (760 mm Hg at sea level), and displacement by water vapor (47 mm Hg for full saturation) and
CO2 . Gas in the alveolus is fully saturated with water vapor, and the amount of alveolar oxygen is further reduced by CO2
that freely diffuses from the pulmonary capillaries in an amount determined by the ratio between oxygen consumption
and CO2 production, termed the respiratory quotient (R), which is affected by diet. On a typical mixed diet, the R is 0.8.
Alveolar oxygen on room air at sea level has a P AO2 = 0.21 x (760 47) Pa CO2 /0.8 (Formula 65-2). The A-a gradient
at sea level for room air is P(A-a)O2 = 149 Pa CO2 /0.8 Pa O2 (Formula 65-3). A simplified formula often used is
P( A-a) O 2 = 145 PaCO2 PaO 2 . A normal P( A-a) O 2 is <10 mm Hg in young, healthy patients, and increases
with age, predicted by the formula P( A-a) O 2 = 2.5 + 0.21 (age in years) (11). The normal A-a gradient is the
value for healthy, asymptomatic individuals measured in an upright or sitting position. The supine position alone, as well
as many chronic cardiac or pulmonary diseases, may raise the A-a gradient. Thus, many patients seen in the ED already
have an elevated A-a gradient due to position or underlying chronic diseases, making it difficult to evaluate increases in
the gradient that may be due to an acute pathologic condition.
Formula 65-2
Formula for determining P AO2 on room air, at sea level.
Formula 65-3

Formula for determining A-a gradient on room air, at sea level.
Formula 65-4
Simple formula for calculating A-a gradient.
Formula 65-5
Simple formula for calculating A-a gradient corrected for age.
Pathophysiology
Hypoxemia results from any combination of five distinct mechanisms.
1. Hypoventilation. Regardless of its cause, hypoxemia from hypoventilation alone is always associated with an
increased Pa CO2 and a normal A-a O2 gradient. In the case of pure hypoventilation, the additional CO2 displaces
inhaled oxygen in the alveolus. Alveolar oxygen, however, diffuses and mixes normally into the arterial blood, as
long as there is no alveolar or interstitial disease.
2. Right-to-left shunt. Right-to-left shunting occurs when blood enters the systemic arteries without traversing
ventilated lung. There is always a small degree of right-to-left shunting because of the direct left ventricular
return of deoxygenated blood from both the coronary veins and the bronchial arteries. Increased right-to-left
shunting occurs in a variety of conditions, including pulmonary consolidation, pulmonary atelectasis, and vascular
malformations. Regardless of the specific cause of the right-to-left shunt, it is always associated with an
increase in the A-a O2 gradient. Right-to-left shunting does not increase Pa CO2 , and patients with a right-to-left
shunt may have an abnormally low Pa CO2 because of hyperventilation. A hallmark of significant right-to-left
shunting is the failure of arterial oxygen levels to increase in response to supplemental oxygen.
Although a small improvement may be observed with supplemental oxygen, hypoxemia is never fully eliminated
because of the mixing of deoxygenated blood in the systemic circulation.
3. Ventilation-perfusion ( / ) mismatch. Ideal pulmonary gas exchange depends on a balance of ventilation and
perfusion. Any abnormality resulting in a regional alteration of either ventilation or perfusion can adversely affect
pulmonary gas exchange, resulting in hypoxemia. There are many causes of / mismatch, including pulmonary
emboli, pneumonia, asthma, COPD, and even extrinsic vascular compression. Regardless of cause, hypoxemia
from ventilation-perfusion mismatch is associated with an increased A-a O2 gradient, and hypoxemia improves
with supplemental oxygen.
4. Diffusion impairment. Pulmonary gas exchange also depends on diffusion across the alveolarblood barrier.
Regardless of the specific cause of the diffusion impairment, the A-a O2 gradient is increased, and hypoxemia
improves with supplemental oxygen.
5. Low inspired oxygen. Decreased ambient oxygen pressure results in hypoxemia. This is most commonly seen
at high altitude or in nonobstructive asphyxia. The A-a O2 gradient is normal, and hypoxemia improves with
supplemental oxygen. For example, Denver, at 5400 ft (1646 m) above sea level, has an atmospheric pressure
of 620 mm Hg and an inhaled P O2 of only 0.21 x 620 = 130 mm Hg, as opposed to 160 mm Hg at sea level.
There are three distinct acute compensatory mechanisms for hypoxemia. Initially, minute ventilation increases. Next,
pulmonary arterial vasoconstriction decreases perfusion to hypoxic alveoli. Although vasoconstriction balances ventilation
and perfusion to restore arterial oxygenation, it may also cause acute right CHF and is ineffective with diffuse lung
disease. Finally, sympathetic tone increases and improves oxygen delivery by increasing cardiac output, usually with an
increased heart rate. Chronic compensatory mechanisms include an increased red blood cell mass and decreased tissue
oxygen demands. These compensatory mechanisms appear to be activated at different levels of hypoxemia for different
individuals. However, the acute compensatory mechanisms are always activated when Pa O2 reaches 60 mm Hg, and
compensatory mechanisms fail when Pa O2 falls below 20 mm Hg.
Clinical Features

The signs and symptoms of hypoxemia are nonspecific. CNS manifestations include agitation, headache, somnolence,
coma, and seizures. Although tachypnea and hyperventilation are often present, at a Pa O2 <20 mm Hg, there is a central
depression of respiratory drive. Cyanosis is not a sensitive or specific indicator of hypoxemia. Patients with chronic
compensatory mechanisms may display polycythemia or alterations in body habitus (e.g., pulmonary cachexia). Using a
combination of clinical signs, it is possible to predict hypoxemia in children with acute respiratory tract infections with
reasonable accuracy, 14 but these predictors have not been validated in adults.
Diagnosis
Hypoxemia is defined as a Pa O2 <60 mm Hg, so formal diagnosis requires ABG analysis. Although pulse oximetry is useful
for screening purposes and decreased Sa O2 readings accurately predict significant hypoxemia, clinically acceptable pulse
oximetry saturation readings (>90%) do not exclude hypoxemia. If Hb is in a state in which it is unable to bind to oxygen
(e.g., methemoglobin or carboxyhemoglobin), pulse oximetry analysis not only overestimates the oxygen saturation but
also reflects a diminished response to any supplemental oxygen (see the section Cyanosis, below).
Treatment
Regardless of the specific cause of hypoxemia, the initial approach remains the same: ensuring a patent airway and
providing supplemental oxygenation with a goal of maintaining a Pa O2 >60 mm Hg. Except in patients with right-to-
left shunts, arterial oxygenation responds to supplemental oxygen.


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HYPERCAPNIA
Hypercapnia is exclusively caused by alveolar hypoventilation and is arbitrarily defined as a Pa CO2 >45 mm Hg. Alveolar
hypoventilation has many causes, including rapid shallow breathing, small tidal volumes, underventilation of the lung, or
reduced respiratory drive. Hypercapnia is never a result of increased CO2 production (Table 65-3).
Table 65-3 Differential Diagnosis of Consequence: Hypercapnia
Depressed central respiratory drive
Structural central nervous system disease: brainstem lesions
Drug depression of respiratory center: opioids, sedatives, anesthetics
Endogenous toxins: tetanus
Thoracic cage disorders
Kyphoscoliosis
Morbid obesity
Neuromuscular impairment
Neuromuscular disease: myasthenia gravis, Guillain-Barr syndrome
Neuromuscular toxin: organophosphate poisoning, botulism
Intrinsic lung disease associated with increased dead space
Chronic obstructive pulmonary disease
Upper airway obstruction
Pathophysiology
A portion of each tidal volume remains in the nongas-exchange portion of the respiratory systemtermed the "dead
space"and is usually determined by the anatomic size of the conducting airways (trachea and bronchi). The portion of
the tidal volume that reaches the alveoli is that which remains after the dead space volume is subtracted: Ta (alveolar
volume) = V T (tidal volume) Td (dead space). Alveolar ventilation (V A) per minute is the volume multiplied by the rate:
V A = Ta x R = (VT Td) x R. Alveolar hypoventilation can result from a decrease in respiratory rate, a decrease in V T , or
an increase in dead space. Under some conditions, dead space volume can increase above that due to the anatomic size
of the conducting airways. Dead space volume increase is a result of ventilation of lung portions with deficient or absent
perfusion, as ventilated portions do not participate fully in gas exchange because of inadequate blood flow.
Because the medullary chemoreceptors stimulate both respiratory rate and V T in response to increased CO2 , alveolar
ventilation is finely controlled relative to the production of CO2 to maintain the Pa CO2 within a narrow range. Decreased
respiratory drive is associated with CNS lesions and toxic depression (Table 65-3). Thoracic cage and neuromuscular
disorders produce hypoventilation by slowing respiratory rate and/or decreasing V T relative to the production of CO2 .
Intrinsic lung diseases, such as COPD, produce alveolar hypoventilation because of an increase in dead space.

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Clinical Features
The signs and symptoms of hypercapnia depend on the absolute value of Pa CO2 and its rate of change. Acute elevations
result in increased intracranial pressure, and patients may complain of headache, confusion, or lethargy. With severe
hypercapnia, seizures and coma can result. Extreme hypercapnia can result in cardiovascular collapse, but this is usually
seen only with acute elevations of Pa CO2 >100 mm Hg. As opposed to acute hypercapnia, chronic hypercapnia, even >80
mm Hg, may be well tolerated.
Diagnosis
Diagnosis of hypercapnia requires ABG analysis. The Web site http://www.medcalc.com/acidbase.html provides an online
acid-base calculator that gives an interpretation of an ABG. Depending on other factors, pulse oximetry analysis can be
normal. With acute hypercapnia, the serum bicarbonate level increases slightly as a result of mass action through the
CO2 bicarbonate (HCO 3 ) equilibrium (Formula 65-6): HCO3 increases about 1 mEq/L for each increase of 10 mm Hg
in the Pa CO2 . Patients with chronic hypercapnia have an elevated serum HCO3 concentration due to the renal response
to increased Pa CO2 (Formula 65-7): the serum HCO3 concentration increases about 3.5 mEq/L for each increase of 10
mm Hg in the Pa CO2 .
Formula 65-6
Acute hypercapnia. Relationship between bicarbonate (HCO 3 ) and Pa CO2 .
Formula 65-7
Chronic hypercapnia. Relationship between bicarbonate (HCO 3 ) and Pa CO2 .
Treatment
Treatment of hypercapnia requires maneuvers to increase minute ventilation, both the rate and the V T , as appropriate.
This involves ensuring a patent airway and may require noninvasive ventilation, mechanical ventilation, the use of an
antidote to reverse drug toxicity, or, rarely, the use of a respiratory stimulant such as doxapram.15 The disposition of
hypercapnic patients depends primarily on the underlying cause and severity. In general, patients with hypercapnia that
causes CNS symptoms should be hospitalized. Also, patients with neuromuscular diseaseeither congenital or acquired
who present with acute hypercapnia should be hospitalized. Some COPD patients have chronic hypercapnia and do not
require admission provided they are stable. Conversely, patients with COPD who display worsening hypercapnia despite
maximal therapy require hospital admission. Oxygen therapy required to maintain minimum saturation levels should not
be withheld from COPD patients in an effort to reduce hypercapnia; these patients need noninvasive or invasive assisted
ventilation.


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WHEEZING
Wheezes are adventitious lung sounds that can be best described as "musical," produced by airflow through the central
and distal airways. 16 Wheezes have sinusoidal acoustics, over a wide frequency range, typically 100 to 1000 Hz. The
duration is prolonged, typically >80 milliseconds. Wheezes differ from the other two main adventitial lung sounds: rhonchi
and crackles (rales). Rhonchi are a series of damped sinusoidal sounds of lower frequency (<300 Hz) and prolonged
duration (>100 milliseconds). Crackles are a series of intermittent individual sounds, typically of <20 milliseconds'
duration.
Pathophysiology
The current theory is that wheezes are produced by airway flutter and vortex shedding from the central and distal
airways, although movement of airway secretions may play a small role. Although flutter and vortex shedding are possible
in normal airways, these processes are more pronounced in obstructed airways. Airway obstruction is associated with the
processes of bronchial smooth muscle contraction (bronchospasm), smooth muscle hypertrophy, increased mucus
secretion, and peribronchial inflammation.
Clinical Features
Wheezing is usually associated with asthma and other obstructive pulmonary diseases characterized by bronchial
obstruction caused by muscular spasm and inflammation (Table 65-4). Upper airway obstruction causes stridor, loudest
at the larynx. Wheezing can also occur during quiet inspiration or forced expiration in some normal children and adults.
Patients with severe airflow obstruction may not wheeze.
Table 65-4 Differential Diagnosis of Consequence: Wheezing
Upper airway (more likely to be stridor, may have element of wheezing)
Angioedema: allergic, angiotensin-converting enzyme inhibitor, idiopathic
Foreign body
Infection: croup, epiglottis, tracheitis
Lower airway
Asthma
Transient airway hyperreactivity (usually caused by infection or irritation)
Bronchiolitis
Chronic obstructive pulmonary disease
Foreign body
Cardiovascular
Cardiogenic pulmonary edema ("cardiac asthma")
Noncardiogenic pulmonary edema (acute respiratory distress syndrome)
Pulmonary embolus (rare)
Psychogenic

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Diagnosis
Airflow obstruction can be assessed with bedside spirometry, by measuring PEF or forced expiratory volume in 1 second
(FEV 1 ). Accurate measurement requires a cooperative patient and usually three maximal-effort expirations. Severely
dyspneic patients and children may not be able to perform the maneuver. The obtained maximum value should be
compared to predicted normal values for age, gender, and height. Predicted normal values are not greatly affected by
weight or ethnicity. PEF or FEV1 values >80% of the predicted value are within the normal range. Values between 50%
and 80% of predicted constitute mild airflow obstruction, values between 25% and 50% constitute moderate airflow
obstruction, and values <25% constitute severe airflow obstruction. However, the severity of clinical symptoms depends
upon the rapidity of the development of obstruction as well as the FEV1 . Relief of symptoms is correlated more closely
with the relative degree of airflow improvement than with the absolute PEF or FEV1 . A significant change in PEF or FEV1 is
more than 8% to 10% from one measurement to another.
Spirometry can be used to screen for possible hypercapnia in adults with acute asthma. Values <25% of predicted suggest
possible hypercapnia, but values >25% essentially exclude it. Unfortunately, there are no spirometric values that can be
used to screen for hypercapnia in COPD patients.
A chest radiograph may or may not be useful in assessing wheezing, but is more useful for patients without a history of
asthma. Patients with COPD and CHF who present with significant dyspnea and wheezing should have chest radiographs
to evaluate for severity and complications.
ABG analysis is useful if the clinical assessment suggests hypoxemia, hypercapnia, or metabolic acidosis. The ABG
analysis may also provide baseline values for further testing and treatment. However, most patients with mild to
moderate asthma and wheezing can be assessed by spirometric analysis and do not require routine ABG analysis.
Treatment
Treatment of wheezing is directed by the underlying disorder and often involves aerosols of 2 agonists (e.g., albuterol)
and/or anticholinergics (e.g., ipratropium bromide). Patients with peribronchial inflammation are often treated with
systemic (PO or IV) or inhaled steroids (see Chapter 72, Acute Asthma in Adults, and Chapter 73, Chronic Obstructive
Pulmonary Disease).


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COUGH
Cough is a protective reflex for clearing secretions and foreign debris from the tracheobronchial tree. 17 Coughing is
initiated by stimulation of irritant receptors located largely in the larynx, trachea, and major bronchi. These receptors are
stimulated by inhaled irritants (e.g., dust), allergens (e.g., ragweed pollen), toxic substances (e.g., gastric acid), hypo- or
hyperosmotic liquids, inflammation (e.g., asthma), cold air, instrumentation, and excess pulmonary secretions. Minor
cough receptors located in the upper respiratory tract (sinuses and pharynx) and chest (pleura, pericardium, and
diaphragm) may stimulate coughing. Signals from these receptors travel by means of the vagus, phrenic, and other nerves
to the cough center in the medulla.
Once stimulated, the cough center initiates the stereotypical cough pattern: a deep inspiration followed by attempted
expiration against a closed glottis that suddenly opens, providing for a forceful exhalation of gas, secretions, and foreign
debris from the tracheobronchial tree. The coughing sound is generated at the larynx and resonates in the nasal cavity
and the lungs. 17
Coughing patterns vary widely according to the underlying status of the lungs, the presence or absence of secretions, and
whether the cough is voluntary or involuntary. Thus, the frequency, duration, and quality of coughing varies among
patients.
Clinical Features
Acute cough is cough lasting <3 weeks and is usually associated with self-limited infectious upper respiratory
or bronchial infections (Table 65-5). Subacute cough lasts 3 to 8 weeks and is most commonly postinfectious, but
causes of subacute cough overlap with causes of acute and chronic cough. Chronic cough is present for >8 weeks.
The term "upper airway cough syndrome" is now used instead of the term "postnasal drip syndrome."
Table 65-5 Differential Diagnosis of Consequence: Cough
Acute Chronic Chronic: Less Common
Upper respiratory infection: rhinitis, Smoking and/or chronic bronchitis Heart failure
sinusitis, pertussis
Bronchiectasis
Lower respiratory tract infection: Postnasal discharge (upper airway Lung cancer or other intrathoracic
bronchitis, pneumonia cough syndrome) mass
Asthma: reactive airways disease Emphysema
Allergic reaction Gastroesophageal reflux Occupational and environmental

irritants
Asthma Angiotensin-converting enzyme Recurrent aspiration or chronic foreign

inhibitor body
Environmental irritants
Transient airway hyperresponsiveness Angiotensin II receptor blocker Psychiatric
Foreign body Postinfectious; pertussis Miscellaneous: cystic fibrosis,

interstitial lung disease

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ACUTE COUGH
Acute cough is most often caused by upper respiratory tract infection, lower respiratory tract infection, and allergic
reactions. Common upper respiratory infections are associated with a combination of rhinorrhea, sinusitis, pharyngitis, and
laryngitis, with the cough a result of drainage from the nasopharynx onto cough receptors in the pharynx and larynx. A
productive cough is the hallmark of acute bronchitis. Although pneumonia generally produces a cough, pulmonary
secretions may be scant and the cough nonproductive. Pertussis in adults has been associated with acute cough lasting 1
to 6 weeks. The incidence of pertussis in adolescents and young adults has increased 400%, accounts for approximately
half of all cases, and is thought to be due to waning vaccine immunity with increasing age. 18
SUBACUTE COUGH
Postinfectious cough is the most likely cause of subacute cough. The mechanisms include postviral airway inflammation
with bronchial hyperresponsiveness, mucus hypersecretion, upper airway cough syndrome (postnasal drip), or asthma.
CHRONIC COUGH
The most common causes of chronic cough are (1) smoking, often with chronic bronchitis; (2) upper airway cough
syndrome (formerly postnasal discharge); (3) asthma; (4) gastroesophageal (GE) reflux; and (5) angiotensin-converting
enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) therapy (Table 65-5).1921 Smoking-induced coughing
is usually worse in the morning and, with chronic bronchitis, usually productive. Upper airway cough syndrome, formerly
called postnasal drip syndrome, is associated with mucus drainage from the nose, a history of "allergies or sinus
problems," and frequent clearing of the throat or swallowing of mucus. The postnasal drainage itself may not only directly
stimulate a cough, but the conditions producing postnasal drainage (e.g., allergic rhinitis) may also cause irritation or
inflammation of upper airway structures that directly stimulate cough receptors independently of the drainage. Chronic
cough associated with asthma is usually worse at night, exacerbated by irritants, and associated with episodic wheezing
and dyspnea. Asthma can be exacerbated by -blocker therapy and presents with nocturnal coughing. Cough associated
with GE reflux often has a history of heartburn, is worse when lying down, and improves with anti-acid therapy (antacids,
H 2 blockers, or proton-pump blockers).
COUGH FROM ANGIOTENSIN-CONVERTING ENZYME INHIBITORS AND

ANGIOTENSIN II RECEPTOR BLOCKERS
The incidence of ACE inhibitor cough is approximately 10% to 12%, although higher values have been published.22 All
ACE inhibitors and ARBs can induce cough, and it is not clear whether certain agents have a higher likelihood of inducing
cough than others. ACE inhibitor cough is thought to result when the blockade of ACE leads to accumulation of bradykinin
and substance P, which stimulate the pulmonary cough receptors and enhance the formation of irritating prostaglandin
metabolites. The onset of ACE inhibitor cough is highly variable: early (1 week) or later (1 year) onset after starting
treatment, only slightly bothersome to debilitating symptoms, and variation during the day.
Diagnosis
Most causes of acute cough do not warrant ancillary tests. A chest radiograph may be used in patients with purulent
sputum and/or fever, and spirometry can document the presence of airflow obstruction in patients with asthma. Pertussis
is diagnosed by culture for Bordetella pertussis with nasopharyngeal swabs, or serologic testing.
Patients with chronic cough should be referred to a primary care physician or an appropriate specialist for definitive
diagnosis.
Treatment
ACUTE COUGH
In addition to disease-specific therapy, patients with acute cough may benefit from antitussives, which block the cough
reflex at various locations. The effectiveness of dextromethorphan or codeine for cough has been questioned by small
studies, 23,24 but opioid antitussives are still recommended on a short-term basis.25 Slow-release morphine sulfate (5 to
10 milligrams twice a day) decreases cough and cough-related symptoms.26 Although cough suppressants are usually

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restricted to patients with a dry cough and avoided in patients with significant sputum production, there is only tradition
to support this practice. Demulcents, part of most proprietary cough preparations, soothe the pharynx and somewhat
suppress the cough reflex. Of the herbal agents, menthol and the pungent spices (e.g., pepper, mustard, garlic, radish,
and onions) have an antitussive effect. 27 For intractable coughing paroxysms in the ED, 4 cc of 1% or 2% preservative-
free lidocaine (40 or 80 milligrams) can be delivered by nebulization. This can cause transient suppression of the gag
reflex due to posterior pharyngeal anesthesia. Pertussis is treated with macrolide antibiotics or trimethoprim-
sulfamethoxazole for 7 days. Because it is highly contagious, those exposed to active cases should also be treated.
SUBACUTE AND CHRONIC COUGH

The main goal is to determine if the subacute and chronic cough is postinfectious or not. If it is, then it must be
determined if it is a result of transient bronchial hyperresponsiveness, asthma, pertussis, upper airway cough syndrome,
pneumonia, or an acute exacerbation of chronic bronchitis. Treatment is then directed at the presumed cause. If the cause
is not postinfectious, it is evaluated and treated in the same manner as a chronic cough. 25
Because chronic cough is most often the result of a few common disorders, an algorithmic approach to treatment using
sequential steps appears to be effective 20,25,28 (Figure 65-1.1):
1. Reduce exposure to lung irritants (e.g., smoking) and discontinue ACE inhibitors, ARBs, and -blockers.
2. Treat for postnasal discharge with an oral first-generation antihistamine/decongestant with or without an
inhaled nasal steroid. If the cough improves, continue treatment and evaluate for sinus disease with imaging
studies.
3. Evaluate and treat for asthma.
4. Obtain chest and sinus imaging if not already done.
5. Evaluate and treat for GE reflux.
6. Refer the patient for specialist evaluation, for CT of the chest and evaluation for pulmonary and nonpulmonary
causes of cough, or bronchoscopy.
Figure 65-1.1.
Evaluation of subacute and chronic cough for patients 15 years of age and older. ACEI = angiotensin-converting enzyme inhibitor;
A/D = antihistamine/decongestant; GERD = gastroesophageal reflux disease; ICS = inhaled corticosteroids; LTRA = leukotriene
receptor antagonist; NAEB = nonasthmatic eosinophilic bronchitis; PPI = proton pump inhibitor; UACS = upper airway cough
syndrome. (Data from Irwin RS, Baumann MH, Boulet LP, et al: Diagnosis and management of cough: executive summary. ACCP
evidence-based clinical practice guidelines. Chest 129: 1S, 2006.)
By using a sequential approach, >95% of patients achieve resolution of their cough. 28
Practice Guidelines
Comprehensive evidence-based practice guidelines for the diagnosis and management of cough have been developed by
the American College of Chest Physicians and their recommendations are summarized in Figure 65-1.1 (see
http://www.chestjournal.org.libproxy1.nus.edu.sg/cgi/content/full/129/1_suppl/1S for the full guidelines). 25


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HICCUPS
Hiccup, or singultus, is involuntary spastic contraction of the inspiratory muscles. Hiccups have no specific protective
purpose.29
Pathophysiology
The afferent arm of the hiccup reflex consists of the phrenic and vagus nerves as well as the thoracic sympathetic chain.
There is no well-defined central hiccup center; instead, there is an intensive interconnection among the hypothalamus,
medullary reticular formation, respiratory center, and cranial nerve nuclei. The efferent limb of the reflux uses the phrenic
nerve, the recurrent laryngeal branch of the vagus nerve, and the motor nerves to the anterior scalene and intercostal
muscles.
Inspiration normally inhibits glottic closure and maintains an open airway. During swallowing, the stimulation of glottic
closure inhibits inspiration, preventing aspiration. In some manner, the hiccup reflex disrupts the connection between
these two processes so that 30 to 40 milliseconds after the onset of inspiration, glottic closure is stimulated. In most
cases in which a specific cause can be assigned, hiccups appear to result from stimulation, inflammation, or injury to one
of the nerves of the reflex arc.
Clinical Features
Hiccups are classified as benign and self-limited or persistent and intractable (Table 65-6).29
Table 65-6 Differential Diagnosis of Consequence: Hiccups
Acute: Benign, Self-Limited Chronic: Persistent, Intractable
Gastric distention Central nervous system structural lesions
Alcohol intoxication Vagal or phrenic nerve irritation
Excessive smoking Metabolic: uremia, hyperglycemia
Abrupt change in environmental General anesthesia

temperature
Psychogenic Surgical procedures: thoracic, abdominal, prostate and urinary tract,

craniotomy
Foreign body in ear touching tympanic membrane (especially hair)
Benign hiccups are generally initiated by gastric distention from food, drinking (especially carbonated beverages), or air.
Alcohol ingestion appears to precipitate hiccups by relaxing the relationship between inspiration and glottic closure,
making it easier for other stimuli to trigger the reflex.
Persistent hiccups are usually a result of injury or irritation to a branch of the vagus or phrenic nerves. One rare but
readily treatable stimulus is a foreign body (often a hair) in the external auditory canal that is pressing against the
tympanic membrane and stimulating the auricular branch of the vagus nerve. Several drugsusually steroids and
benzodiazepinesare implicated in inducing hiccups, but the evidence is weak. 30

Diagnosis
The evaluation of persistent hiccups should start with a history to determine whether a specific event was associated with
the onset (Table 65-6). Are the hiccups persistent during sleep? Persistence during sleep suggests an organic cause, and
resolution during sleep suggests a psychogenic cause, although this distinction is not absolute. The external auditory canal
should be carefully examined for foreign body. A chest radiograph should be done to evaluate for intrathoracic pathology.
Fluoroscopy can be useful to evaluate for unilateral versus bilateral diaphragmatic movement during hiccups, but is not
part of the ED evaluation. Unilateral movement suggests focal injury to the phrenic nerve on the affected side.
Treatment
A wide variety of physical maneuvers and medications have been used to terminate an acute episode of hiccups (Tables
65-7 and 65-8).
Table 65-7 Treatment of Hiccups: Physical Maneuvers
Remove foreign body from ear
Swallow a teaspoon of sugar
Sip ice water
Drink water quickly
Table 65-8 Treatment of Hiccups: Drug Treatment
Drug Initial Dose Maintenance Dose
Chlorpromazine 2550 milligrams IV, repeat in 24 h if 2550 milligrams PO three to four times
needed a day
Metoclopramide 10 milligrams IV or IM 1020 milligrams PO three times a day

for 10 d
Haloperidol 25 milligrams IM 14 milligrams PO three times a day
Nifedipine 1020 milligrams PO 1020 milligrams PO three to four times

a day
Valproic acid 15 milligrams/kg PO 15 milligrams/kg PO three times a day
Baclofen 10 milligrams PO 10 milligrams PO three times a day
Gabapentin (for suspected neurologic 100 milligrams 100 milligrams PO three times a day
cause)
Many of these measures are based on the concept that stimulating the pharynx will block the vagal portion of the reflex
arc and abolish the hiccups. 31 No one method appears to be more effective than another. Swallowing a teaspoon of dry
granulated sugar is about as effective as others and does not involve the infliction of noxious or painful stimulation.
Drug treatment (Table 65-8) also works by inhibiting the reflex arc.31
A large number of agents have been described as effective, but mostly only through case reports. Of the recommended
drugs, only chlorpromazine has enough published experience to achieve U.S. Food and Drug Administration approval for
treatment of intractable hiccups. Chlorpromazine and metoclopramide take effect within 30 minutes. Adverse effects
include extrapyramidal symptoms with both agents and hypotension with chlorpromazine. Nifedipine, valproic acid, or
baclofen are options for the primary care physician who will provide continuing care and monitor for adverse effects.



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CYANOSIS
Cyanosis is a bluish color of the skin and mucous membranes that results from an increased amount of reduced Hb
(deoxyhemoglobin) or Hb derivatives. The detection of cyanosis is highly subjective and is not a sensitive indicator of the
state of arterial oxygenation, as cyanosis is determined by the absolute amount of deoxygenated Hb in the blood, not the
amount of oxygenated Hb. Cyanosis is divided into central or peripheral cyanosis. Central cyanosis is cyanosis of
mucous membranes and tongue and is due to inadequate pulmonary oxygenation or an abnormal Hb.
Peripheral cyanosis is cyanosis of the fingers or extremities from vasoconstriction and diminished peripheral
blood flow. All conditions that cause central cyanosis also result in peripheral cyanosis. The distinction into central and
peripheral cyanosis is not possible in conditions where both mechanisms are present (Table 65-9).
Table 65-9 Differential Diagnosis of Consequence: Cyanosis
Central Cyanosis Peripheral Cyanosis
Hypoxemia Reduced cardiac output
Decreased fraction of inspired oxygen: high altitude Cold extremities
Hypoventilation Maldistribution of blood flow:

distributive forms of shock
Ventilationperfusion mismatch Arterial or venous obstruction
Right-to-left shunt: congenital heart disease, pulmonary arteriovenous fistulas,

multiple intrapulmonary shunts
Abnormal skin pigmentation
Heavy metals: iron, gold, silver, lead, arsenic
Drugs: phenothiazine, minocycline, amiodarone, chloroquine
Hemoglobin abnormalities
Methemoglobinemia: hereditary, acquired
Sulfhemoglobinemia: acquired
Carboxyhemoglobinemia (not true cyanosis)
Clinical Features
Traditional teaching has been that cyanosis is usually present when deoxygenated Hb exceeds 5 grams/dL. However, this
figure is questionable because central cyanosis can be detected with deoxyhemoglobin concentration as low as 1.5
grams/dL. In some instances, cyanosis can be detected when Sa O2 has fallen to 85%; in others, it may not be detected
until Sa O2 is 75%.
Various physiologic, anatomic, and physical factors other than the amount of reduced Hb may influence the appearance of
cyanosis, making an accurate clinical detection of the degree or even the presence of cyanosis difficult (Table 65-10).
Table 65-10 Factors Influencing the Physical Appearance of Cyanosis

Physiologic factors
Oxygen content of blood
Degree of oxygen extraction
Oxyhemoglobin dissociation curve
Anatomic factors
Status of microcirculation
Skin pigmentation
Skin thickness
Physical factors
Quality/intensity of light in examination area
Skill of examining physician
The tongue and buccal mucosa are thought to be sensitive sites for observing central cyanosis.
Peripheral cyanosis is caused by the slowing of blood flow to an area and an abnormally large extraction of oxygen from
normally saturated arterial blood. CHF, peripheral vascular disease, shock states, and cold exposure all create states of
vasoconstriction and decreased peripheral blood flow, with cyanosis of the nail beds. When cardiac output is reduced,
cutaneous vasoconstriction occurs because blood flow is preferentially distributed to more vital areas. Extremity cyanosis
can be evident even with normal arterial blood oxygenation. Massage or gentle warming of a cyanotic extremity will
increase peripheral blood flow and abolish peripheral, but not central, cyanosis.
Diagnosis
Pulse oximetry can diagnose hypoxemia and provide continuous oxygen saturation measurements. However, an exception
occurs when the Hb is in a state in which it is unable to bind to oxygen (e.g., methemoglobin or carboxyhemoglobin). In
such situations, pulse oximetry analysis not only overestimates the oxygen saturation but also reflects a
diminished response to any supplemental oxygen. In the setting of methemoglobinemia, pulse oximetry will read
80% to 85% regardless of the degree of methemoglobinemia, thereby overestimating the true oxygen saturation (it may
be lower, but pulse oximetry will not read lower). With carboxyhemoglobinemia, the pulse oximetry reads
carboxyhemoglobin as oxyhemoglobin (see Chapter 201, Dyshemoglobinemias, and Chapter 217, Carbon Monoxide).
ABG analysis with co-oximetry (a specific measurement of oxygen saturation) is still the gold standard in the assessment
of any patient with suspected cyanosis. In central cyanosis, the oxygen saturation measured from the ABG is decreased
because of the underlying hypoxemia. In peripheral cyanosis, assuming normal cardiopulmonary and Hb status, the
oxygen saturation should be normal. If methemoglobinemia or carboxyhemoglobinemia is suspected, the ABG analysis will
show a normal Pa O2 (reflecting a normal amount of dissolved oxygen in the plasma), a normal calculated oxygen
saturation (from the normal Pa O2 ), and a decrease in measured oxygen saturation (because of a decreased number of
oxygen binding sites). If the measured Pa O2 and the Hb concentration are normal, the cyanosis may be a result of
abnormal skin pigmentation or abnormal Hb (see Chapter 201, Dyshemoglobinemias, and Chapter 217, Carbon
Monoxide).
Treatment
Patients with central cyanosis should be given supplemental oxygen, and the underlying disorder should be treated.
Failure to improve suggests impaired circulation (shock), abnormal Hb, or pseudocyanosis. See Chapter 201,
Dyshemoglobinemias, and Chapter 217, Carbon Monoxide Poisoning, for details of treatment for dyshemoglobinemias or
carbon monoxide poisoning.



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PLEURAL EFFUSION
Pleural effusions result from fluid accumulating in the potential space between the visceral and parietal pleurae. Although
pleural effusions can result from many causes, in developed countries the most common causes are CHF, pneumonia, and
cancer (Table 65-11).
Table 65-11 Differential Diagnosis of Consequence: Pleural Effusion
Common Less Common
Transudates
Heart failure Cirrhosis with ascites
Peritoneal dialysis
Nephrotic syndrome
Exudates
Cancer: primary or metastatic Viral, fungal, mycobacterial, or parasitic infection
Bacterial pneumonia with parapneumonic Systemic rheumatologic disorders: systemic lupus erythematosus,
effusion rheumatoid arthritis
Pulmonary embolism Uremia, pancreatitis
Postcardiac surgery or radiotherapy
Drug-related: amiodarone
Either transudates or exudates
Transudates after diuretic therapy Pulmonary embolism
Pathophysiology
Normally, a small amount of fluid is secreted from the parietal pleura into the pleural space where it is absorbed by the
visceral pleural microcirculation. This small amount of pleural fluid reduces friction between the pleural layers and allows
for smooth lung expansion and contraction with respiration. Any process that increases fluid production or interferes with
fluid absorption will result in accumulation in the pleural space. Pleural effusions are traditionally divided into exudates or
transudates based on mechanism. 30 Exudative effusions result from pleural disease, usually inflammation or neoplasia,
that results in active fluid secretion or leakage with high protein content. Transudative effusions result from an imbalance
between hydrostatic (e.g., CHF) and oncotic (e.g., nephrotic syndrome) pressures. This imbalance results in the
production of an ultrafiltrate with low protein content across the pleural membrane.
Clinical Features
A pleural effusion may be clinically silent or come to detection from either symptoms of an underlying disease, an increase
in volume of the effusion with the production of dyspnea, or the development of inflammation and associated pain with
respiration. Physical findings of a pleural effusion include percussion dullness and decreased breath sounds. Because
pleural fluid typically pools in the dependent portions of the hemithorax, small or moderate size effusions have percussion

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dullness and decreased breath sounds at the lung base with relatively normal lung findings above the level of fluid. With
large or massive effusions, it may be impossible to distinguish a fluid level on clinical examination.
Diagnosis
In an adult, 150 to 200 mL of pleural fluid in the hemithorax is required to produce signs on upright chest radiography.
Supine chest radiographs may demonstrate only a hazy appearance of pleural fluid in the posterior pleural space (Figure
65-2A). CT scanning of the chest may clarify uncertain findings on chest radiograph (Figure 65-2B). Small free-flowing
pleural effusions can be visualized on decubitus radiographic views (Figure 65-3). US can be used to image pleural
effusions, although accuracy depends on operator technique and the quality of interpretation. A significant pleural
effusion is large enough to produce a pleural fluid strip >10 mm wide on lateral decubitus radiographic views
or by ultrasonography.32
Figure 65-2.

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A. This is a supine radiograph showing a right-sided pleural effusion. The right lung field is hazy compared to the left, and a small
layer of fluid is noted inferiorly. B. CT scan of the patient in (A). A moderate pleural effusion is noted in the right lung field, and a
small effusion not seen in the left lung field of the plain film is noted on the CT scan.
Figure 65-3.

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Left lateral decubitus radiograph showing a layering of a small pleural effusion. Arrowhead points to the layer of fluid.
Diagnostic thoracentesis is done to obtain pleural fluid for analysis in cases without a clearly evident cause, to confirm a
suspected diagnosis, or to detect pleural space infection. For example, because the largest single cause of pleural effusion
is CHF, if a patient presents with a typical appearance (cardiomegaly, roughly equal in size bilateral effusions), then a
period of treatment with monitoring for pleural fluid resolution is indicated, and routine thoracentesis is reserved for those
patients who do not resolve in 3 to 4 days. Otherwise, diagnostic thoracentesis and pleural fluid analysis is indicated.
Light and colleagues developed the most widely used criteria to differentiate transudates from exudates using serum and
pleural fluid protein and lactate dehydrogenase levels (Table 65-12).32 Several modifications to the original criteria have
been proposed.33 Regardless, the sensitivity of these criteria for the detection of an exudative pleural effusion is 98% to
99% with specificity from 65% to 86%. If the clinical circumstances suggest that the effusion is likely to be transudative,
the only tests indicated are pleural fluid and serum protein content and lactate dehydrogenase levels. If the pleural
effusion is exudative, additional tests are indicated (Table 65-12).32
Table 65-12 Pleural Fluid Diagnostic Tests
Detection of exudative pleural effusion
Light32 and colleagues' criteria for pleural exudate: one or more of the following present: (modified)
Pleural fluid/serum protein ratio >0.5
or
Pleural fluid/serum LDH ratio >0.6

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or
Pleural fluid LDH greater than two thirds of the upper limit for serum LDH
Additional tests on exudative effusions
Gram stain and culture to detect bacterial infection
Cell count
Neutrophil predominance: parapneumonic, pulmonary embolism, pancreatitis
Lymphocytic predominance: cancer, tuberculosis, postcardiac surgery
Glucose: low glucose seen in parapneumonic, malignant, tuberculosis, and rheumatoid arthritis causes of pleural
effusions
Cytology for malignancy: highest yield is with adenocarcinoma, much lower with squamous cell, lymphoma, or
mesothelioma
Pleural fluid pH: normal pleural fluid pH around 7.64. In parapneumonic effusions, a pleural fluid pH <7.10 predicts
development of empyema or persistence and indicates need for thoracostomy tube drainage.
Pleural fluid amylase: elevated in pleural effusions due to pancreatitis or esophageal rupture
Mycobacterial and fungal stains and cultures: as suggested clinically
Tuberculosis pleural fluid markers: polymerase chain reaction for mycobacterial DNA, pleural fluid adenosine deaminase,
or pleural fluid interferon-
Abbreviation: LDH = lactate dehydrogenase.
The distinction between exudates and transudates may be obscured by the effect of diuretic therapy in patients with
transudative pleural effusions. During diuresis, the resorption of water is faster than that of protein, so the protein
concentration rises into the range consistent with an exudative etiology. A serum to pleural albumin difference of >1.2
grams/dL has been proposed to help in this scenario, but this approach will reduce the sensitivity of exudative pleural
effusion detection by >10%. 32,33
Treatment
If the patient has dyspnea at rest, therapeutic thoracentesis with drainage of 1.0 to 1.5 L of fluid is indicated. Acute
drainage of larger volumes has been associated with reexpansion pulmonary edema, and drainage of larger volumes is to
be avoided. Patients with pleural empyema (gross pus or organisms on Gram stain) require drainage with large-bore
thoracostomy tubes. Treatment of parapneumonic effusions is controversial (see also Chapter 69, Empyema and Lung
Abscess). Clinical findings that suggest the need for thoracostomy tube drainage for parapneumonic effusion include
comorbid disease, failure to respond to antibiotic therapy, anaerobic organisms, pleural fluid pH <7.10, and effusion
involving >50% of the thorax or air-fluid level on the chest radiograph. 34 Diuretic therapy typically resolves >75% of
effusions due to CHF within 2 to 3 days.


AccessMedicine | Print: References
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Useful Web Resources

American College of Chest Physicians Guidelines for Diagnosis and Management of Cough
http://www.chestjournal.org.libproxy1.nus.edu.sg/cgi/content/full/129/1_suppl/1S
National Lung Health Education Program pleural effusion sitehttp://www.nlhep.org/books/pul_Pre/pleural-effusion.html
Breath sound audio, including wheezinghttp://www.medspan.info/articles/clinical-medicine/tips-for-respiratory-

auscultation-with-audio-examples-of-lung-sounds.html or http://www.wilkes.med.ucla.edu/lungintro.htm


Respiratory Distress Patient Tintinalli 7th Ed

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Stimulation of upper airway mechanical and thermal receptors

Decreased stimulation of chest wall afferents

Stimulation of central hypercapnic chemoreceptors in the central medulla

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Table 65-1 Differential Diagnosis of Consequence: Dyspnea

Most Common Causes Most Immediately Life-Threatening

Heart failure/cardiogenic pulmonary edema Tension pneumothorax

Ischemic heart disease: unstable angina and myocardial Pulmonary embolism

Psychogenic Fat embolism

DIFFERENTIATING CARDIAC FROM PULMONARY CAUSES OF DYSPNEA

Table 65-2 Factors Supporting Heart Failure as the Cause of Dyspnea

Finding LR + (95% CI) LR (95% CI)

Clinical gestalt 4.4 (1.810.0) 0.45 (0.280.73)

Heart failure 5.8 (4.18.0) 0.45 (0.380.53)

Myocardial infarction 3.1 (2.04.9) 0.69 (0.580.82)

Coronary artery disease 1.8 (1.12.8) 0.68 (0.480.96)

Paroxysmal nocturnal dyspnea 2.6 (1.54.5) 0.70 (0.540.91)

Orthopnea 2.2 (1.23.9) 0.65 (0.450.92)

Edema 2.1 (0.925.00) 0.64 (0.391.10)

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Dyspnea on exertion 1.3 (1.21.4) 0.48 (0.350.67)

S 3 gallop 11.0 (4.925.0) 0.88 (0.830.94)

Jugular venous distention 5.1 (3.27.9) 0.66 (0.570.77)

Hepatojugular reflex 6.4 (0.8151.00) 0.79 (0.621.00)

S4 1.6 (0.475.50) 0.98 (0.931.00)

Wheezing 0.52 (0.380.71) 1.3 (1.11.7)

Pulmonary venous congestion 12.0 (6.821.0) 0.48 (0.280.83)

Interstitial edema 12.0 (5.227.0) 0.68 (0.540.85)

Alveolar edema 6.0 (2.216.0) 0.95 (0.930.94)

Cardiomegaly 3.3 (2.44.7) 0.33 (0.230.48)

Atrial fibrillation 3.8 (1.78.8) 0.79 (0.650.96)

Any abnormal finding 2.2 (1.63.1) 0.64 (0.470.88)

B-type natriuretic peptide <80 picograms/mL 0.06 (0.030.13) 3.3 (1.86.3)

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B-Type Natriuretic Peptide

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Formula for calculating tissue oxygenation.

Formula for determining P AO2 on room air, at sea level.

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Formula for determining A-a gradient on room air, at sea level.

Simple formula for calculating A-a gradient.

Simple formula for calculating A-a gradient corrected for age.

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Table 65-3 Differential Diagnosis of Consequence: Hypercapnia

Depressed central respiratory drive

Structural central nervous system disease: brainstem lesions