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336 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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Inequality of pulses. Disparity between right and left arterial pulse volumes
is detected by simultaneous palpation and conrmed by taking the blood
pressure at both sites. Arterial pressure differences between the arms must
be interpreted cautiously: pressures not measured precisely simultaneously
are >10 mm Hg different in up to 20% of normal individuals, whereas, when
measured simultaneously by cuff, 5% or less show the same difference. Nonsimultaneously measured systolic pressure differences of >10 mm Hg occur
in almost 30% of hypertensive patients. Asymmetry suggests atherosclerosis,
dissecting aneurysm or another arterial disease.
Dysrhythmias. See Chapter 4, page 57. Many dysrhythmias produce arterial beats of variable volume and disordered timing. Evaluate the disturbance
from the precordial ndings rather than the peripheral pulse. Ventricular contraction before the ventricle has had time to ll produces a peripheral pulse
wave of diminished volume, or none at all. The ECG, not palpation or ausculta-
tion, is the only way to accurately diagnose rhythm disturbances.
Arterial Murmur or Bruit. Normal arteries are silent when auscultated.
Turbulence is heard as a murmur and palpated as a thrill. Although murmur
and bruit are literally synonymous, there is a tendency to reserve bruit for
arterial sounds. The presence of a bruit does not necessarily indicate limited
ow. Arteries become tortuous from arteriosclerosis or other circumstances
and dilate with aneurysm. They may be constricted congenitally, by intimal
proliferation, or by an atherosclerotic plaque. Dilated thyroid arteries with
increased blood ow occur in Graves disease (here, the word bruit is often
used). Blood ow through an arteriovenous stula or large arterial collaterals, as in aortic coarctation, often produces bruits. A continuous murmur is
produced by an arteriovenous stula or a partially obstructed artery when
the collateral circulation is poor, and the diastolic pressure is low distal to the
obstruction.
Carotid bruit. Most of the blood ow to the brain and virtually all to the cerebral cortex comes through the internal carotid arteries. Despite collateral ow
through the circle of Willis from the contralateral carotid and vertebrobasilar
system, high-grade obstruction of one common and/or internal carotid artery
is associated with high risk of disabling stroke. The neck should always be
auscultated for bruits, and bruits should be evaluated by imaging. The degree
of stenosis cannot be estimated by physical exam. Symptoms of cerebral ischemia in the distribution of the affected artery are associated with a substantial
risk for stroke within hours to days.
Arterial sound—pistol-shot sound.
wave front of higher than normal pulse pressure striking the arterial wall in
the region being auscultated. When the stethoscope bell is placed lightly over
an artery, particularly the femoral, a sharp sound like a gunshot is heard. Although commonly associated with aortic regurgitation, it also occurs in other
conditions with high pulse pressure, e.g., hyperthyroidism and anemia.
Duroziez sign. Compressing the femoral artery with the stethoscope bell produces eddies and a systolic bruit. Continue listening while pressure on the
bell is gradually increased. If, with further pressure a point is reached where
This is produced by an arterial pulse
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a second murmur becomes audible, it is Duroziez sign. Most commonly encountered in severe aortic regurgitation, it occurs in other conditions with a
high pulse pressure (Chapter 4, page 68). The second murmur is associated
with an exaggerated forward acceleration of blood ow.
Venous signs of cardiac action. Cardiac action produces signs in the venous
system by altering peripheral venous pressure and pulse contour and by producing venous congestion in the viscera.
Elevated CVP.
exceeding venous capacitance and/or impedance to lling of the right atrium or right ventricle. Impedance to right ventricular lling is often due to
impaired outow from the right ventricle causing elevated right ventricular
end-diastolic pressure.
ter under resting conditions, it is considered elevated. DDX: A generalized
increase in venous pressure must be distinguished from SVC and/or IVC
obstruction. Always assess whether the venous pressure appears uniformly
elevated above and below the diaphragm; it must be if the CVP is elevated.
Absence of signs below the diaphragm suggests SVC obstruction [Cook DJ,
Simel DL. The rational clinical examination. Does this patient have abnormal
central venous pressure? JAMA. 1996;275:630–634].
CLINICAL OCCURRENCE: Overlling of the Vascular Space: Kidney failure,
rapid infusion of uids and blood products, chronic CHF with edema;
Impedance to Right Heart Filling: Tricuspid stenosis or regurgitation, peri-
cardial tamponade, constrictive pericarditis; Impaired Right Ventricular
Outow: Pulmonary hypertension, pulmonary embolus, pulmonic stenosis,
right ventricular infarction.
Diminished venous pressure. This occurs in peripheral circulatory failure in
the shock syndrome, usually associated with intravascular hypovolemia, diminished venous tone, and/or peripheral pooling. The peripheral veins are
collapsed with the patient supine. See the discussion of Hypotension, Chapter 4, page 67.
Giant a-waves—tricuspid stenosis. See page 332.
Cannon a-waves. Right atrial contraction against a closed tricuspid valve
produces retrograde ejection of blood into the central venous channels.
termittent prominent venous pulsations are visible in the neck veins, cannon
a-waves. They are identied as a-waves, since they are asynchronous with the
apical impulse and carotid upstroke. They are easily obliterated by gentle
pressure at the base of the neck insufcient to diminish the carotid pulse.
DDX: Irregular cannon a-waves suggest that some atrial contractions are
occurring simultaneously with ventricular contraction. A regular pattern of
cannon a-waves suggests a xed pattern of AV block, e.g., atrial utter with
2:1 block. An irregular pattern with variable a-wave volume suggests AV dissociation, e.g., complete heart block. An ECG is required to diagnose the rhythm.
Regular giant a-waves occurring consistently in synchrony with the heart
sounds and arterial pulse suggests impedance to right atrial outow, e.g., a
noncompliant right ventricle or tricuspid stenosis.
Elevated CVP indicates overlling of the intravascular space
When the venous pressure exceeds 10–12 cm of wa-
In-
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Large v-waves in the venous pulse—TR. Tricuspid insufciency allows the
right ventricle to eject blood retrogradely into the central venous channels.
Large v-waves are visible in the jugular veins and may be palpable as liver
pulsation. The waves are v-waves since they are synchronous with the apical
impulse and carotid upstroke.
Kussmaul sign and hepatojugular reux.
accommodate increased venous return gives rise to these signs.
the patient so the jugular blood column is just visible above the clavicle.
Kussmaul sign is present if the venous column doesn’t collapse during
inspiration. Next, with the patient breathing normally, place the right hand
on the right upper abdominal quadrant pressing rmly upward under the
costal margin for ≥10–15 seconds. Hepatojugular reux is present if the jugular venous column rises and persists while abdominal pressure continues.
Hepatojugular reux is most commonly seen with early right heart failure.
Both are seen with severe right heart failure, constrictive pericarditis, and
right ventricular infarction.
Arterial Circulation Signs: Decreased arterial blood ow causes skin pallor,
coldness, and tissue atrophy. Small-vessel pathology is often recognizable by
cutaneous manifestations (page 288 and Chapter 6, page 127). Diseases affecting small arteries and arterioles, e.g., vasculitis, tend to be diffuse. Diseases of
larger vessels cause regional hypoperfusion.
Warm skin. Normal skin temperature indicates adequate arterial ow.
Normal nailbed color is red or pink.
Sharply demarcated warm and cool, pallid digits. Raynaud Syndrome.
Raynaud syndrome occurs as the result of severe cutaneous arterial spasm
most commonly in the ngers but may also occur in the ears, nose and toes.
The primary manifestations are sharply demarcated cyanosis followed by
pallor and numbness and painful parasthesias involving the affected area.
As vasospasm resolves over minutes to hours, the skin may become erythematous and the pain intensies before resolving. Raynaud’s syndrome
may occur idiopathically or secondarily in autoimmune disease and is often
provoked by exposure to cold or emotional distress.
The right heart's inability to
Position
Atheroembolic disease. Embolization of cholesterol-rich atheroma to the
small arteries produces hemorrhagic cutaneous infarcts and livedo.
Palpable purpura—vasculitis. See Leukocytoclastic Vasculitis, page 363.
Skin pallor and coldness—chronic arterial obstruction. Chronic progressive
arterial obstruction induces collateral circulation and tissue accommodation
to ischemia. Pallid cool skin strongly suggests regional hypoperfusion. It
is normal in a cold environment but should rapidly resolve on exposure to
warm air or water. Failure to do so suggests that the problem is not limited to
the skin vessels but involves a major trunk artery. Pain may be present with
exertion (claudication). The distribution of the arterial decit depends upon
the site of obstruction and the presence and extent of collateral circulation.
Other useful signs are prolonged venous lling time, abnormal pedal pulses
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and a femoral bruit. Atherosclerosis is most common; less common causes are
large vessel vasculitis (Takayasu aortitis, giant cell arteritis), Buerger disease,
vasospastic disorders, and ergotism.
Dependent rubor and coldness—chronic arterial obstruction. See Examination of the Arterial Circulation in the Extremities, page 287, and Chronic
extremity peripheral vascular disease, page 374.
Acute pain, skin pallor, and coolness—arterial embolus or thrombosis.
Acute occlusion of a major peripheral artery resulting in cutaneous and muscular ischemia produces skin and nailbed pallor, cool skin, and ischemic pain.
The pain is severe and not relieved by changing position. Embolic arterial
occlusion is most common in native vessels, whereas thrombus is more common in prosthetic vascular channels. Urgent relief of obstruction is necessary
to preserve the part. See acute extremity artery obstruction, page 374. The
heart is the most common source of emboli (endocarditis, prosthetic valve,
atrial brillation). Less commonly, an embolus arises from thrombus within
an aortic aneurysm or paradoxical embolism via a patent foramen ovale.
Nodular vessels—polyarteritis nodosa. See page 362.
CHEST, CARDIOVASCULAR, AND RESPIRATORY SYNDROMES
Chest Wall Syndromes.
Chest pain intensied by respiratory motion. Pain accentuated by breathing, coughing, laughing, or sneezing usually indicates inammation or injury
to the ribs, cartilages, muscles, nerves, and pleurae of the chest wall. The specic area may also be tender. See Chest Wall Pain with Tenderness, page 301,
as there is signicant overlap between these categories.
Pleuritis and pleurisy. The parietal pleura has sensory bers from the in-
tercostal nerves that also give off twigs to the skin. The visceral pleura is
anesthetic. Pleural pain is caused either by stretching of the inamed parietal
pleura or by separation of brous adhesions between two pleural surfaces.
It is doubtful that pain is produced by the pleural surfaces rubbing together
as pain often occurs without a friction rub and a rub is often present without
pain.
Pleural inammation (pleuritis) produces knife-like shooting chest wall
pain intensied by breathing, coughing, and laughing. Listen and palpate for
a friction rub. Rubs are not constant, so frequently repeat the exam. Pleural
effusion may develop. The diagnosis of pleurisy is made from the typical pain
or the presence of a friction rub after excluding other causes of pleuritis, rib
fractures, myositis, and neuritis. Pleurisy and a rub may precede radiographic evidence of pneumonia. Common causes of pleurisy include bacterial and
viral pneumonia, tuberculosis, empyema, viral pleuritis, pulmonary infarction from embolus, mesothelioma, primary and metastatic lung neoplasm,
and connective tissue diseases.
Diaphragmatic pleuritis and pleurisy. The peripheral diaphragmatic pleura
is supplied by the fth and sixth intercostal nerves so pain is felt near the costal margins. The central diaphragm (thoracic and peritoneal) is innervated by
the phrenic nerve (C3–4), which also innervates the neck and supraclavicular
340 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
Pain from central diaphragm
Pain from peripheral diaphragm
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FIG. 8-43 Referral of Left Diaphragmatic Pain.
fossae. Thus, pain in the neck and supraclavicular region may result from irritation of the diaphragmatic pleura (Fig. 8-43). There is sharp shooting pain
intensied by deep breathing, coughing, or laughing. Pain may be localized
along the costal margins, epigastrium, lumbar region, or neck at the superior
border of the trapezius or supraclavicular fossa, always on the same side.
A pleural or pericardial friction rub may be present.
pleurisy is suggested when pain is accompanied by fever and a friction rub.
Pleural effusion may appear later. A history of dysphagia, nausea or intraabdominal disease suggests disorders of the esophagus, pancreatitis, subphrenic abscess, peptic ulcer, splenic infarction or splenic rupture. Hiatal hernia
can produce similar pain. Pericarditis with pleuritic pain (pleuropericarditis)
should be considered.
DDX: The diagnosis of
Epidemic pleurodynia (Bornholm disease, devil's grip). Infection with group
B coxsackievirus is a common cause. After a nonspecic prodrome, the
patient is suddenly seized with sharp, knife-like thoracic or abdominal pain,
intensied by breathing and movement, and accompanied by fever. The chest
may be splinted, and the thighs exed on the belly. Paroxysms of intense pain
are separated by intervals of complete comfort. Cases are sporadic or epidemic. Mild pharyngitis and myalgias with tenderness of the neck, trunk, and
limbs may be present. A friction rub is detected in 25% of cases. The sudden
retrosternal pain suggests MI or dissecting aneurysm.
Chest wall twinge syndrome (precordial catch). The patient experiences brief
episodes of nonexertional sharp pain or “catches” in the anterior chest, usually on the left side. Some patients report onset while bending over. The pains
last from seconds to minutes and are aggravated by deep breathing and relieved by shallow respirations. The cause is unknown. The condition is common and harmless.
Rib fracture, periosteal hematoma, periostitis, intercostal myositis. See page
301.
Respiratory Syndromes.
Pneumothorax. Spontaneous rupture of a subpleural bleb, penetrating chest
trauma and medical procedures may allow air to enter the pleural space
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separating the lung and chest wall leading to failure of respiratory mechanics and lung collapse.
by dyspnea and severe chest pain that is often unilateral but poorly localized. Vital sign changes are proportional to the degree of collapse and concurrent cardiopulmonary disease and include tachypnea, tachycardia and
hypotension. With a large pneumothorax, the physical signs are distinctive:
hyperresonant percussion, markedly diminished or absent fremitus, voice
transmission, and breath sounds on the affected side, and tracheal deviation away from the affected side (page 311). Respiratory rib movements are
decreased with persistent expiratory distention of the hemithorax. When tension pneumothorax develops, hemodynamic shock may occur within minutes and urgent diagnosis and treatment are necessary to prevent death. With
a small pneumothorax, the only sign may be decreased breath sounds. On
chest X-ray, lung markings are absent and often the visceral pleura is seen
as a line. On thoracic ultrasound, pneumothorax is detected by noting the
absence of sliding pleura and normal ultrasound reverberation through in the
lung tissue. Tension pneumothorax is a hemodynamic diagnosis and when
suspected must be managed prior to obtaining conrmatory X-rays.
CLINICAL OCCURRENCE: Pneumothorax results from rupture of a pleu-
ral bleb in pulmonary emphysema, and, occasionally, from inammatory
lung disease, such as sarcoidosis, brosis, or silicosis. Primary spontaneous
pneumothorax is most often described in slender, healthy young persons
with no discernible pulmonary lesion. Alveolar and pleural inammation
and necrosis secondary to septic embolism in bacterial endocarditis or pneu-
mocystis jiroveci infection in HIV/AIDS may cause pneumothorax. Puncture
of the lung by a fractured rib is the most common traumatic cause. In hospital-based settings, pneumothorax may be secondary to complications of
mechanical ventilation (barotrauma), as well as procedural complications
during central venous catheter placement, pacemaker insertion and lung
biopsy procedures. The differential diagnosis of the sudden pain, dyspnea
and hemodynamic changes must be distinguished from PE, MI, and acute
pericarditis.
Large sudden pneumothoraces may be accompanied
Acute bronchitis. Acute infection is usually viral, an atypical organism being
less common. Airway inammation produces persistent cough often with
retrosternal burning pain. Fever is absent. Secretions in the bronchi and trachea produce rhonchi and, occasionally, wheezing. Secretions high in the trachea produce rhonchi that are heard throughout the thorax. The cough may
be unproductive or tenacious, mucoid sputum may be raised. Usually, the
airways are unimpaired so breath sounds are normal.
inuenza, and RSV are common. Chest X-ray is normal.
Pneumonia. Lung infection and inammation are labelled pneumonitis or
pneumonia. The process may be limited to the airways and alveolar airspaces
or involve the pulmonary interstitium and vascular channels. The diagnostic
challenges are to separate infectious from noninfectious pneumonia and then
to identify the specic etiology. Key patient factors that determine risk for
pneumonia as well as likely pathogens include immune status, age, tobacco
use, inhalational exposures and preexisting lung disease. Onset is sudden or
gradual, depending upon the etiology. Patients present with cough, dyspnea,
fatigue, and, especially with infection, high fever, often with rigors. Physical
DDX: Inuenza, para-
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ndings range from minimal signs of airspace disease (bronchophony, whispered pectoriloquy) to respiratory failure with multilobar consolidation.
Infectious pneumonia is separated into community-acquired and hospitalhealthcare-associated categories. The approach to diagnosing specic etiologies of pneumonia is beyond the scope of this text.
CLINICAL OCCURRENCE: Congenital: Pulmonary sequestration (may
be confused with pneumonia on chest X-ray);
Idiopathic interstitial pneumonia, eosinophilic pneumonia, alveolar proteinosis; Infectious: Bacterial, viral, tuberculosis, nontuberculous mycobacteria, rickettsia, fungi, Nocardia, pneumocystis, parasites; Inammatory/
Immune: Hypersensitivity pneumonitis, vasculitis, lymphomatoid granu-
lomatosis, Goodpasture syndrome, lipoid pneumonia, collagen vascular diseases; Mechanical/Traumatic: Aspiration, lung contusion; Metabolic/
Toxic: Inhalational injury, drug reactions, pneumoconioses; Neoplastic:
Endobronchial neoplasm with post-obstructive infection, bronchioloalveolar cell carcinoma; Vascular: Vasculitis (Churg-Strauss, granulomatosis with
polyangiitis).
Severe acute respiratory syndrome (SARS) and middle east respiratory syndrome (MARS). Infection with coronaviruses cause severe lung
inammation leading to hypoxia and respiratory failure. The SARS outbreak in 2003 originated in China and spread rapidly but was controlled.
In 2012 a different coronavirus causing the same syndrome was identied in Saudi Arabia and the Near East and entered the US in 2014.
initial u-like illness is followed rapidly progressing pneumonia. The
case fatality rate is high. Spread is by droplets. To make the diagnosis,
a high index of suspicion is necessary with careful questioning about
contact with infected or potentially infected people and travel to known
areas of ongoing transmission. Current information is available at the
Centers for Disease Control web site, www.cdc.gov.
Degenerative/Idiopathic:
An
Aspiration pneumonia. Aspiration of oral secretions, food, or regurgitated
stomach contents causes mechanical airway obstruction with secondary inammation (especially with low-pH gastric contents) and secondary infection often with anaerobic oral ora. The right middle and apical segment
of the right lower lobe are commonly affected. Aspiration is common in association with impaired consciousness or swallowing. Coughing with meals
and nocturnal regurgitation with cough and dyspnea suggest chronic aspiration. Necrotizing anaerobic infections lead to lung abscess with fetid
sputum. Aspiration should be suspected when a patient presenting with
pneumonia has a history of impaired consciousness or oropharyngeal neurologic dysfunction.
Lung abscess. Necrotizing organisms destroy lung tissue creating cavities
with low oxygen tension, ideal for growth of microaerophilic or anaerobic
organisms. A history compatible with aspiration is often present. The sputum
is scant to intermittently copious, purulent, and foul smelling. Signs of consolidation may be present. If the cavity communicates with a bronchus and
is only partially lled amphoric breath sounds may be heard (see Fig. 8-34,
page 308). A fungus ball occurs when an old abscess cavity is colonized with
Aspergillus.
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Bronchopleural stula with empyema. Bronchopleural communication is
caused by an empyema draining through a bronchus or a lung abscess eroding into the pleural space. The presentation is chronic cough producing a
large volume of purulent sputum. Sudden entry of pus into the pleural space
produces severe prostration, chills, fever, and/or shock. Dullness with absent
breath sounds in the lower hemithorax and a resonant region above—the
whole devoid of breath sounds—suggests the diagnosis. A succussion splash
may be heard.
Pulmonary embolism. A dislodged deep vein thrombus (DVT) passes
through the RA and RV into the pulmonary circulation. Large emboli
obstruct the main pulmonary artery at its bifurcation or one of its branches
producing acute pulmonary hypertension which in turn causes right
ventricular pressure overload and RV failure with cardiogenic shock.
Lung infarction initiates local inammation. Ventilation–perfusion mismatching and intrapulmonary shunts cause hypoxia. DVT develops after
surgery (particularly total hip and knee replacement), prolonged bed rest
and air travel, immobilization, and venous stasis. Thrombophilia (factorV Leiden, prothrombin gene mutations, antiphospholipid syndrome,
protein C or S deciency, mucinous adenocarcinomas, estrogens, pregnancy, etc.) increases DVT risk. Less-commonly embolized material are
fat (from the marrow of fractured bones), air, amniotic uid (when the
uid contains meconium, it is especially dangerous), and tumor tissue.
Patients may be minimally symptomatic or present with sudden dyspnea, chest pain, and circulatory failure. Symptoms: Sudden dyspnea,
with or without pain or tachypnea, is the key symptom. The pain is
either pleuritic or a deep, crushing sensation in the six-dermatome band.
Sometimes painless dyspnea resembles asthma because of the release of
serotonin from platelets in the blood clot. Massive pulmonary embolus
presents as syncope without other symptoms.
Signs: Systemic effects
(weakness, prostration, sweating, nausea, and vomiting) may predominate. Tachycardia is nearly always present. Fever occurs with infarction.
Dyspnea, tachypnea, and cyanosis can be extreme. Hemoptysis, a pleural
friction rub, and bloody pleural effusion strongly support PE with infarction. Massive infarction is indicated by shock, jaundice, and right-sided
heart failure. A loud P2 and palpable precordial RV thrust indicate pulmonary hypertension. Sudden death is not uncommon. Occasionally, PE
is accompanied by abdominal rigidity because the diaphragm is splinting adjacent to infarcted lung. A high index of suspicion is necessary
to aggressively pursue the diagnosis as the next embolus may be fatal.
Chronic recurrent pulmonary emboli lead to pulmonary arterial hypertension. DDX: Sudden onset of chest pain and/or dyspnea, tachypnea,
or unexplained sinus tachycardia should raise the question of PE with or
without infarction. The symptoms and signs may suggest asthma, bronchopneumonia, pleurisy, pericarditis, spontaneous pneumothorax, MI,
acute pancreatitis, or perforated peptic ulcer.
Sleep-disordered breathing—obstructive and central sleep apnea. Sleep-
disordered breathing results from either mechanical obstruction by redundant, lax oropharyngeal soft tissues (obstructive sleep apnea) or from decreased
medullary respiratory drive (central sleep apnea). Hypoventilation and hypoxia
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at night produce frequent arousals, disrupting effective sleep. Patients are
often, but not always, obese. They have daytime hypersomnolence and irritability and frequently have morning headaches and hypertension. Snoring
is prominent but may not have been noted by the patient so history from
the bed partner is critical. In prolonged disease, hypertension and fatigue or
depression may be severe. Chronic nocturnal hypoxia leads to pulmonary
hypertension and right heart failure. Physical risk factors for obstructive
apnea are enlarged tongue, thickened oropharyngeal soft tissues (Mallampati
score 3 or 4, Chapter 7, page 231) or neck circumference >43 cm (17 inches) in
men or >40.5 cm (16 inches) in women.
Chronic cough. Patients present with chronic irritating cough and normal
physical ndings. Ninety percent of cases are caused by chronic postnasal drip, unsuspected asthma, and/or gastroesophageal reux; evaluation
for each is required. Angiotensin-converting enzyme inhibitors also cause
chronic cough, which may begin months after starting the medication.
Pleural effusion. See page 308.
Lung cancer. Most primary lung cancers result from cigarette smoking or
exposure to ionizing radiation.
related to the chest (cough, hemoptysis, dyspnea, pneumonia, pleural effusion), regional symptoms (lymphadenopathy, SVC syndrome, brain mass), or
systemic symptoms (weight loss, weakness, hypercalcemia, hyponatremia).
Endobronchial lesions present as recurrent or slowly resolving pneumonia
or atelectasis. Bronchioloalveolar cell carcinoma presents with cough, hypoxia,
and diffuse inltrates, often mistaken for infection. Superior sulcus tumors
(neoplasms in the pulmonary apex, the upper mediastinum, or the superior
thoracic aperture) produce Pancoast syndrome with severe neck, shoulder or
arm pain.
Pulmonary edema. LV failure, mitral regurgitation, or acute lung injury
result in interstitial pulmonary edema and alveolar ooding. An acute
increase in LV end-diastolic pressure is transmitted across the mitral valve
to the left atrium and pulmonary veins. Increased hydrostatic pressure in the
pulmonary capillaries causes transudation of uid into the pulmonary interstitium and subsequently the alveoli. Increased uid in the lung decreases
pulmonary compliance producing shortness of breath and cough. Alveolar
ooding causes hypoxia and extreme respiratory distress. Severe dyspnea
is accompanied by crackles, rhonchi, and gurgles throughout the lungs.
Breathing is labored, with cyanosis and frothy sputum, often pink, occasionally bloody. Percussion is resonant, and auscultation reveals bubbling crackles and sometimes wheezes.
is often relapsing making the diagnosis obvious. It may occur suddenly with
acute MI, especially with papillary muscle rupture and ail mitral valve leaflet. Occasionally, paroxysmal nocturnal dyspnea in cardiac patients closely
resembles asthma with prolonged expiration and wheezing.
CLINICAL OCCURRENCE: Degenerative/Idiopathic: High altitude; Infectious:
Hantavirus pulmonary syndrome; Inammatory/Immune: Mismatched blood
transfusion, hypertransfusion syndrome, SLE; Mechanical/Traumatic: LV
failure-systolic and diastolic dysfunction (MI, cardiomyopathies, tachy- and
Patients present with symptoms and signs
DDX: In chronic heart failure pulmonary edema
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bradyarrhythmias), mitral stenosis, mitral and aortic insufciency (especially acute), PE, head trauma;
tion of noxious gases, aspiration, radiation, hemorrhagic pancreatitis, sepsis,
drugs, fresh water drowning, etc.), intravenous heroin, snakebite; Neoplastic:
Bronchioloalveolar cell carcinoma (not pulmonary edema, but may appear
similar radiographically), lymphangitic carcinoma or lymphoma; Neurologic:
Postictal, head trauma, subarachnoid hemorrhage;
sion, intravascular volume overload (crystalloid, colloid, transfusions, kidney failure), subarachnoid hemorrhage.
Interstitial lung disease.
edema, and/or collagen deposition thickens the alveolar walls and septa,
decreases lung compliance, reduces lung volume, and impairs gas exchange.
Inammation may involve the entire alveolus. Granulomas, characteristic of
some diseases, are diagnostically important.
nonproductive cough and dyspnea. Thorough occupational and avocational
exposure histories are critical to identifying respiratory irritants, toxins,
and allergens. Physical exam shows resonant percussion, decreased breath
sounds, and crackles of varying intensity, often at end-inspiration and usually
most prominent at the bases. Chest X-ray shows increased interstitial markings, with or without alveolar signs. High-resolution CT may be diagnostic
with characteristic patterns for specic entities.
CLINICAL OCCURRENCE: Congenital: Tuberous sclerosis, neurobromato-
sis, Niemann–Pick disease, Gaucher disease; Degenerative/Idiopathic: Idiopathic
interstitial pneumonia (usual interstitial pneumonia), desquamative interstitial pneumonia, respiratory bronchiolitis-associated interstitial lung disease,
acute interstitial pneumonia, cryptogenic organizing pneumonia, nonspecic
interstitial pneumonia; after acute respiratory distress syndrome, radiation;
lymphangioleiomyomatosis, amyloidosis,
tissue diseases (SLE, RA, ankylosing spondylitis, systemic sclerosis, CREST
syndrome [calcinosis cutis, Raynaud phenomenon, esophageal motility disorder, sclerodactyly, and telangiectasia], Sjögren syndrome, polymyositis–
dermatomyositis) eosinophilic pneumonia, antibasement membrane disease
(Goodpasture), idiopathic pulmonary hemosiderosis, graft-versus-host disease, with gastrointestinal or liver disease (Crohn disease, ulcerative colitis,
primary biliary cirrhosis, chronic active hepatitis); Metabolic/Toxic: Inhaled
substances (asbestosis, fumes and gases, aspiration pneumonia); with granulomas (hypersensitivity pneumonitis—organic dusts, e.g., farmer’s lung,
inorganic dusts—beryllium, silica); Drugs (antibiotics, amiodarone, gold,
bleomycin, and other chemotherapy agents).
Metabolic/Toxic: Acute lung injury (inhala-
Vascular: Severe hyperten-
Inammation with cellular inltration, interstitial
Patients present with chronic
Inammatory/Immune: Connective
Hypersensitivity pneumonitis. Exposure to organic dusts at work or home
elicits a chronic inammatory response which can progress to irreversible
brosis. Careful history is the key to diagnosis. Patients present with cough,
shortness of breath, and increasing dyspnea, often with airow obstruction on exposure to the agent. Exam may be normal or reveal crackles and
wheezes.
Pulmonary-renal syndromes. There are antibodies to basement membrane
in the glomerulus and pulmonary capillaries (Goodpasture), or vasculitis
involving the lung and glomeruli (granulomatosis with polyangiitis) each
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