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286 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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the CVP height collapses the distal veins. Transient distention of the jugular
veins is seen with increased intrathoracic pressure as with coughing, laughing, crying, and Valsalva. Also, a large cervical or retrosternal goiter may
cause venous obstruction.
Estimating CVP. The vertical distance in centimeters from the head of the
jugular blood column to the right atrium is an approximate measure of CVP.
When identiable, the internal jugular vein provides a more accurate estimate
than the external jugular veins; the veins on the right are more reliable than
those on the left. When sitting or standing, distended external jugular veins
indicate an increased CVP (assuming no SVC obstruction). The presence of
jugular venous waves excludes central obstruction. Tense venous distention
may prevent visualization of the venous waves. In any patient with jugular
venous distention, note the presence of facial edema and dilated collateral
vessels on the anterior chest and back indicative of central venous obstruction
and superior vena cava syndrome.
Indirect CVP measurement. If the jugular veins are collapsed in the vertical
position, slowly lower the thorax until the head of the blood column appears.
The right atrial position is estimated by running an imaginary anteroposterior line from the anterior fourth interspace halfway to the back; a horizontal plane through this point is the zero level for measuring venous pressure
(Fig. 8-21B). The vertical distance in centimeters from this plane to the head of
the blood column is the approximate CVP. The angle of Louis (sternal angle)
is another reference point for estimating CVP. It is ~6 cm above the RA in
most positions, though not always. Jugular venous pulsations >3 cm vertically above this landmark indicate elevated venous pressure.
Alternate indirect CVP measurement. Place the patient supine with an arm
hanging over the bedside. Raise the arm slowly until the distended arm or
hand veins collapse. The vertical distance from the zero level to the point of
collapse estimates the CVP. Select a vein as close to the heart, for example, the
cephalic, basilic, or median basilic veins (Fig. 8-22). There is great variation in
the caliber and superciality of the arm veins.
Venous pulsations. The venous pulse wave can be demonstrated in the external jugular veins if not obscured by overlying tissue. Venous pulsation is readily distinguished from an arterial pulse by being impalpable. There are three
upward components to the venous pulse wave (Fig. 8-23) and two prominent
descents. The a-wave results from right atrial systole; the c-wave is principally
caused by expansion of the underlying carotid artery and is usually not visible. The a-wave peak is followed by an x-descent, initially because of atrial
relaxation and later of downward movement of the tricuspid valve with right
ventricular systole. The rising v-wave is produced by right atrial lling with
the tricuspid valve closed. The peak of the v-wave is followed by the y-descent
associated with tricuspid valve opening at onset of right ventricular diastole.
Correctly identifying the waves and descents requires careful correlation with
the cardiac cycle. The rapid descents are usually better appreciated than the
slowly rising waves. The x-descent is normally the most readily observed portion of the jugular pulse, and its nadir is approximated by S2. The peak of the
a-wave is normally the most prominent wave and occurs at about S1.
Physical Exam of The Chest and Major Vessels 287
Biceps brachii m.
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External jugular v.
Median basilic v.
Great saphenous v.
Visible Veins and Venous Pressure Measurements. A. Veins of the neck. B. Veins of the arm .
FIG. 8-22
C. Veins of the thigh and leg.
Venous pulsations are also seen as lateral neck expansion and contraction occurring with lling and collapse of the internal jugular veins and
their tributaries. This is best seen from the foot of the bed. In a few persons,
pulsations occur in the supercial veins of the arms, forearms, and hands. A
disproportion in the number of a-waves and ventricular systoles indicates a
dysrhythmia, but the waves are difcult to see consistently. Failure to identify
an expected venous pulse may indicate obstruction of veins proximal to the
right atrium.
Capillary pulsation. Press down on the tip of a ngernail until the distal third
of the nailbed blanches. With each heartbeat, the border of pink extends and
recedes. This a prominent sign in aortic regurgitation known as Quincke pulse,
but it can be seen to a lesser degree in many normal persons.
Examining the Arterial Circulation in the Extremities: Large named arteries
normally have visible or palpable pulses. Their occlusion is recognized by
regional ischemia. In the complete physical exam, assess the circulation by (1)
bilateral palpation of the pulse volume in brachial, radial, femoral, dorsalis
pedis, and posterior tibial arteries; (2) palpation for skin temperature changes;
(3) inspection for varicose veins, edema, pallor, cyanosis, and ulceration of the
arms and legs; and (4) inspection of the retinal vessels. Complaints of pain,
coolness, or numbness in an extremity or signs of enlarged veins, masses,
swellings, localized pallor, redness, or cyanosis lead to special examinations
288 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
Jugular pulse (sphygmogram)
Q
ECG
Lead
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a
c
v
x
y
S
P
FIG. 8-23 Jugular Venous Pulse Waves. Heart action is reflected in the jugular vein. The waves should be timed
with the apical impulse or heart sounds, remembering that a perceptible time elapses between cardiac events and their signs
in the neck. The a-wave is the rebound from atrial systole. The bulging of the tricuspid valve cusps early in ventricular systole
produ ces the c-deflec tion. The v- wave result s from atrial fi lling while th e valve is closed, togethe r with an upward m ovement of
the AV valve ring at the end of ventricular systole. The x-descent comes with atrial relaxation and the y-descent with opening
of the tricuspid valve.
T
of the peripheral circulation. The cause of a circulatory decit is suggested
by the history, the distribution of the decit, and the state of the vessel wall.
Skin exam for circulation. When a part is below heart level, pooled venous
blood obscures evidence of arterial ow. Venous pressure is rarely >30 cm above
that of the right atrium, whereas the systolic arterial pressure is >120 cm above
the same reference point. Thus, lifting the hand or foot above the right atrium to
a height exceeding the venous pressure, drains the masking venous blood pool
permitting evaluation of tissue color produced by the arterial inow. The most
reliable signs of a regional perfusion abnormality are a temperature or perfusion discrepancy between symmetrical parts at the same external temperature.
Skin color. Color is imparted by blood in the venules of the skin’s subpapillary layer and its melanin content. Examining for circulatory changes in
dark-skinned individuals is difcult. Rather, focus attention on the mucous
membranes, nail beds, and palms. When the arterial ow is nil and the veins
empty, the skin is chalky white. Partial but inadequate arterial supply produces red or cyanotic skin, depending on the effect of external temperature
and amount of pooled blood in the venules.
Skin temperature. Temperature reliably indicates skin perfusion. Normal
ow is principally governed by arteriolar constriction or dilatation. Internal
body temperature is maintained within narrow limits, partly by heat dissipation from the skin. In clothed persons, the skin of the head, neck, and
trunk is warmer than that of the extremities, and the digits are cooler than the
proximal hands and feet. Peculiarly, normal digits adjust their temperature
to only one of the two levels. The ngers are somewhat cooler (32°C [90°F])
than blood temperature (37°C [98°F]) when the air temperature exceeds 20°C
(68°F). If the air temperature is below 16°C (60°F), nger temperatures drop to
approximately 22°C (72°F); no intermediate level is maintained.
Physical Exam of The Chest and Major Vessels 289
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A.
B.
FIG. 8-24
the skin and nail beds. Arterial deficit produces a violaceous color from pooling of the blood in the venules because of
loss of venomotor tone as a result of hypoxia. B. While the patient is supine, the foot is elevated above the level of
venous pressure (15 cm [6 in.] above the right heart or 25 cm [10 in.] above the table when the patient is supine). Elevation
drains the foot of venous blood, so the skin color reflects only the presence of arterial blood. The elevated leg is compared
with the opposite extremity. C. The hand is raised above the heart level, so the skin color is produced exclusively
by arterial blood.
Circulation of the Skin in Extremities. A. The legs are dependent to observe the color of
C.
Examining for arterial decit. In a draft-free room at ~22°C (72°F) the
extremities are normally exposed for 10 minutes while the complete physical
exam is being performed. This duration of exposure can be used to assess the
health of the skin and vasculature in the extremities. Coldness and pallor of
the skin should not be routinely demonstrated with this exposure in normal
patients. Have the patient sit, hanging the legs from the table or bed, comparing the skin color of both feet looking for pallor, deep redness, pale blueness,
deep blueness, or a violaceous color (Fig. 8-24A). With the back of your hand
or ngers feel the skin temperature from the feet up the legs. Compare comparable sites on each leg in sequence noting whether an increase in temperature is gradual or sharply demarcated. Have the patient lie supine. Grasp the
patient’s ankles and elevate the feet >30 cm (12 inch) above the right atrium.
Note any change in skin color (Fig. 8-24C). If the color does not change, have
the patient dorsiex the feet ve or six times, wait several minutes, then
observe the feet for color changes induced by exercise. Allow the feet to hang
down again and note the time for the color to return. Note how quickly color
returns to an area blanched by nger pressure.
Inspect the feet carefully for evidence skin atrophy, loss of lanugo hair on
the dorsa of the toes, thickening or transverse ridging of the nails, and ulceration or patches of gangrene. Examine the arms similarly by exposing them
for 10 minutes and then observing the color in dependency and when elevated
well above heart level (Fig. 8-24B). Repetitively opening and closing the sts
discloses latent color changes. Note the time for color return in dependency.
Examining large arm and leg arteries. Palpate the walls of accessible arteries
for increased thickness, tortuosity, and beading. A spastic artery feels like a
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FIG. 8-25 Testing Patency Arm Arteries. A. Palpable segments of the arm arteries (segments in solid
black). Frequently the ulnar pulse is not palpable in normal persons. B. Allen test. See the text for details.
small cord. Compare the pulse volume at symmetric arterial levels. Be careful
not to mistake the pulse in your own nger for that of the patient.
Doppler ultrasound. Small portable instruments may be used at the bedside
and these can more precisely evaluate the arterial circulation particularly for
patients with signicant peripheral vascular occlusive disease. When pulses
are not palpable, Doppler ultrasound is required to distinguish nonpalpable
ow from total arterial occlusion.
Arms. Listen for a bruit in the supraclavicular fossa over the subclavian artery.
Only the brachial artery in the upper arm and the radial and ulnar arteries at
the wrist are palpable. With the forearm exed 90 degrees, palpate the bra-
chial artery on the medial arm in the groove between the biceps and triceps
muscles (Fig. 8-25A). Palpate the radial artery on the wrist’s exor surface just
medial to the radial styloid. Palpate the ulnar artery on the wrist’s exor surface just medial to the distal ulna; it lies deeper than the radial artery and may
not be palpable. Determine radial and ulnar artery patency with the Allen
test (Fig. 8-25B). With the patient sitting and hands supinated on the knees,
grasp the right wrist, with your thumbs on its exor surface. Have the patient
make a tight st, then compress both the radial and ulnar arteries with your
thumbs. Have the patient open the hand. The skin should be pale and remain
so while both arteries are compressed. Take your thumb off the radial artery;
the palm and ngers should quickly turn pink as ow returns. Delayed ush
or no ush indicates partial or complete radial artery obstruction. Repeat the
process, this time removing pressure from the ulnar artery. Return of ow
is normally somewhat slower from the ulnar artery, but absence of ush is
pathologic. Repeat this sequence on the other hand.
Legs. Palpate the abdominal aorta deeply between the xiphoid and the umbi-
licus. Palpate the common femoral arteries just below the inguinal ligaments,
equidistant between the anterior superior iliac spines and the pubic tubercles (Fig. 8-26). Feel for popliteal artery pulsation with the patient supine and
the legs extended. Place a hand on each side of the patient’s knee with your
thumbs anteriorly near the patella and the ngers curling around so the tips
Physical Exam of The Chest and Major Vessels 291
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FIG. 8-26 Palpable Lower Limb Arteries. The palpable segme nts of the ar teries are in so lid black. The f emoral artery
is palpable only a short distance below the inguinal ligament at the midpoint between the anterior superior iliac spine and the
pubic tubercle. The popliteal artery lies vertically in the popliteal fossa; it can be felt only by compressing the contents of the
fossa from behind against the bone. The posterior tibial artery can be felt as it curls forward and under the medial malleolus.
The palpable segment of the dorsalis pedis artery lies just lateral to the most medial of the dorsal tendons of the foot (the
flexor of the great toe) over the arch of the foot.
rest in the popliteal fossa. Firmly press the ngers against the lower femur or
upper tibia feeling for arterial pulsation. A normal popliteal artery may not
be palpable. Palpate the posterior tibial artery in the groove between the medial
malleolus and Achilles tendon. It may be more easily palpable with the foot
passively dorsiexed. Locate the dorsalis pedis artery on the dorsum of the foot
just lateral to and parallel with the extensor hallucis longus tendon. In normal
persons aged >45 years, either the dorsalis pedis or posterior tibial pulse frequently will not be palpable, but not both in the same foot.
Ankle brachial index. A quantied measure of arterial function is the ankle-
brachial index (ABI). The ABI is calculated from measurements of the systolic
blood pressure in the brachial artery and the posterior tibial and/or the dorsalis pedis artery. The systolic pressure is taken as the ination pressure of a
standard blood pressure cuff that results in total arterial occlusion. The test
is performed after the patient is at rest in the supine position for 10 minutes.
Most commonly, the cessation of arterial pulses are assessed with a handled
Doppler instrument. The ABI is the ratio of the ankle systolic pressure to
the highest right or left brachial systolic pressure. A normal ABI is >0.9–1.4.
An ABI greater than 1.4 indicates noncompliant, calcied arteries found in
advanced atherosclerosis. Occlusive peripheral vascular disease in the lower
extremity is indicated by the degree of abnormality with 0.75 to 0.9 mild,
0.6 to 0.75 moderate, and <0.6 severe ischemia. An ABI <0.5 suggests severe
arterial disease and potential for limb threatening ischemia. Importantly, the
292 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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ABI should be interpreted within the context of clinical signs and symptoms
such as claudication, paresthesias, weakness, and palpation of both the skin
and pulses.
Examining Large Limb Veins: Adequate drainage of blood from the extremi-
ties requires patent veins, muscle contraction to pump blood proximally by
compressing veins, and competent perforating and deep venous valves limiting retrograde ow. Failure of any one of these results in venous stasis which
increases ltration pressure in the distal capillaries and post-capillary venules
producing edema, stasis pigmentation, and/or skin ulceration.
Examining large arm and leg veins. With the patient supine, look for signs of
venous stasis. Have the patient stand and check for dilated arm and leg veins.
Elevate each extremity determining how rapidly the veins collapse; failure to
promptly empty indicates obstruction. If obstruction is present, palpate the
venous walls for hard plugs of thrombus or hard cords of brosis. If patent
varicose veins are present, additional special tests may be used to assess for
incompetent valves.
Laboratory exam of the large limb veins. Techniques such as Doppler ultrasound, impedance plethysmography, venography, and MRI can determine
the patency and valve competence of the large limb veins.
CHEST, CARDIOVASCULAR, AND RESPIRATORY SYMPTOMS
General Symptoms
Chest pain. Chest pain often causes fear of ischemic heart disease, but
has many noncardiac causes. Chest pain occurring without physical signs
requires a careful history to categorize the attributes of pain. Focus on all the
locations where pain is felt and solicit where it is most intense and if the pain
radiates. Specic attention to the effect of exertion and rest on pain intensity is
also important. Chest pain intensity should be quantied on a 10-point scale
and changes over time and with treatment or intervention should be noted.
Remember to evaluate chest pain and most other symptoms using a standard
approach such as PQRST: provocative-palliative factors, quality, region-referral,
severity, and timing. Interpret the characteristics of the chest pain within the
contex of the patient’s risk for major cardiovascular disease by simultaneously assessing the patient’s ischemic cardiac disease risk factors.
Deep retrosternal or precordial pain and the six-dermatome band. See SixDermatome Pain Syndromes, page 350.
wall from the neck to beneath the xiphoid, and extend down the anteromedial aspect of the arms and forearms (Fig. 8-27). The rst four dermatomes
contain sensory afferents from dorsal roots of T1 to T4 and the lower cervical
and upper thoracic sympathetic ganglia. In the ganglia and spinal cord, the
bers communicate with one another superiorly and inferiorly. The mediastinal, thoracic, and abdominal organs are also supplied by sensory afferents
and parasympathetic efferents via the vagus nerve (CN X). The myocardium,
pericardium, aorta, pulmonary artery, esophagus, and mediastinum have
sensory bers in these pathways. Disorders in any of these structures produce
deep, visceral, and poorly localized pain. Spinal segments T5 and T6 receive
Dermatomes T1–T6 cover the chest
Chest, Cardiovascular, and Respiratory Symptoms 293
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FIG. 8-27 The Six-Dermatome Band. Dermatomes T1–T6 form a band covering most of the thorax and extending
down the anteromedial aspect of the arms and forearms. Sensory pathways from the viscera of this entire region are so
interconnected that stimulation of any part can produce the same patterns of chest pain.
sensory bers from the lower chest wall, the diaphragm and its peritoneal
surface, the gallbladder, pancreas, duodenum, and stomach. Injury to these
structures causes deep, visceral, poorly localized pain very similar in quality
to that of the upper band. Deep visceral retrosternal pain in the precordial
region or epigastrium is typical of pain from the structures supplied by spinal
segments T1–T6, including the sympathetics. It is not specic for heart disorders. Neuroanatomy explains the structural basis for this clinical observation.
Pain arising from T1–T4 usually has maximal intensity retrosternally or in the
precordium, often extending with less intensity into the neck and/or down
the anteromedial aspect of one or both arms and forearms. Pain arising in T5
and T6 is most often maximally intense around the xiphoid and/or in the
back inferior to the right scapula, but pain can extend into the T1–T4 distribution through posterior sympathetic connections, making it indistinguishable
from pain arising above the diaphragm. The location of pain only indicates that
its source is somewhere in the six-dermatome band (the myocardium, pericardium,
aorta, pulmonary artery, mediastinum, esophagus, gallbladder, pancreas, duodenum,
stomach, or subphrenic region).
CLINICAL OCCURRENCE: Congenital: Hypertrophic cardiomyopathy;
Endocrine: Retrosternal thyroid; Degenerative/Idiopathic: Esophageal spasm,
gastroesophageal reux; Infectious: Infectious pericarditis and pleuritis,
granulomatous mediastinal lymphadenopathy, myocarditis, subphrenic
abscess; Inammatory/Immune: Esophagitis, pericarditis, sarcoidosis, pleuritis, myocarditis, postcardiotomy syndrome, pancreatitis, cholecystitis, gastritis; Mechanical/Traumatic: Pneumothorax, esophageal rupture, esophageal
obstruction (extrinsic, foreign body, neoplasm, web, or ring), esophageal
diverticulum, gastric perforation; Metabolic/Toxic: Acid or alkali ingestion;
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Neoplastic: Carcinoma (primary or metastatic) of the esophagus, pericar-
dium, lung, mediastinum, pleura; lymphoma; thymoma; teratoma; testicular
cancer; Neurologic: Postherpetic neuralgia, diabetic radiculopathy, intercostal
neuritis;
malingering, Munchausen syndrome;
nary atherosclerosis, spasm, embolism, thrombosis, vasculitis), central pulmonary embolism (PE) and infarction, aortic dissection.
Shortness of breath—dyspnea. Dyspnea is the result of abnormal gas
exchange (decreased oxygenation, hypoventilation, hyperventilation)
and/or increased work of breathing from impaired respiratory mechanics.
Physiologically, dyspnea may result from pulmonary parenchymal disease,
airways disease, pulmonary vascular disease, chest wall and neuromuscular disease as well as disorders of cardiac output including valvular disease,
arrhythmias, cardiomyopathy and constrictive/restrictive pericardial disease. Dyspnea may result from anemia caused by bone marrow and bleeding
disorders as well as metabolic disorders such as metabolic acidosis, sepsis
and hyperthyroidism.
complaint can be shortness of breath, running out of breath, being unable to
take a deep breath, smothering, or chest tightness. Often accompanying dyspnea are tachypnea, increased respiratory excursions (hyperpnea), tense scaleni and sternocleidomastoid, aring alae nasi, and a distressed expression.
Identify associations of dyspnea, e.g., exertion versus dyspnea at rest and on
standing or lying down. Rare patients seem unaware of dyspnea despite having to pause for breath in the middle of a sentence or even when they have
cyanosis or resting tachycardia. These patients may be at risk for death from
disorders such as asthma since they can present for clinical care late in the
course of their disease and in extremis.
anxiety may be present in patients with ventilatory disorders. Psychiatric
symptoms may be early and dominant features of cardiopulmonary disease. Acutely, hypoxemia and respiratory acidosis may cause delirium and
abnormal behavior. For patients with chronic cardiopulmonary disease such
as chronic obstructive pulmonary disease, pulmonary brosis or congestive
heart failure, the rate of psychiatric comorbidity is high and these patients
should be screened for this psychiatric co-morbidity. Conversely, because of
direct effects on respiratory drive and symptom perception, primary psychiatric disorders such as anxiety as well as some pain syndromes may also
result in profound sensations of dyspnea. Indicators of primary psychiatric
disease include disproportionately severe symptoms compared to physical
ndings, normal lung auscultation, normal pulse oximetry, normal ECG and
normal chest X-ray.
altitude; Airway Obstruction—Larynx and Trachea: Infections (laryngeal diph-
theria, acute laryngitis, epiglottitis, Ludwig angina), angioedema, trauma
(hematoma or laryngeal edema), neuropathic (abductor paralysis of vocal
cords), foreign body, tumors of the neck (goiter, thyroid and thymus carcinoma, primary tracheal tumors, lymphoma), extrinsic compression by aneurysm or esophageal tumor, ankylosis of the cricoarytenoid joints; vocal cord
dysfunction syndrome;
Psychosocial: Somatization disorder, panic attack, hypochondriasis,
Vascular: Myocardial ischemia (coro-
Dyspnea means difcult breathing, both a symptom and a sign. The
Signicant comorbid psychiatric disease including depression and
CLINICAL OCCURRENCE: Decreased Fraction of Inspired Oxygen: high
Bronchi and Bronchioles: Acute and chronic bronchitis,
Chest, Cardiovascular, and Respiratory Symptoms 295
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asthma, retrosternal goiter, aspirated foreign bodies, bronchiectasis, bronchial
stenosis;
inltration (infectious and aspiration pneumonia, carcinoma, sarcoidosis,
pneumoconioses), pulmonary hemorrhage, pulmonary alveolar proteinosis;
Alveolar Destruction: Pulmonary emphysema, pulmonary brosis, cystic dis-
ease of the lungs;
thorax, abdominal distention;
of the respiratory muscles (especially the intercostals and the diaphragm),
myasthenia gravis thoracic deformities (kyphoscoliosis, thoracoplasty),
scleroderma or burns of the thoracic wall, pulmonary brosis;
Pulmonary Circulation: Pericardial tamponade, pulmonary artery stenosis,
arteriovenous shunts in heart and lungs, pulmonary thromboembolism and
infarction, other emboli (fat, air, amniotic uid), arteriolar stenosis (primary
pulmonary hypertension, irradiation);
carbon monoxide poisoning (carboxyhemoglobinemia), methemoglobinemia and sulfhemoglobinemia, cyanide and cobalt poisoning; Abnormal
Respiratory Stimuli: Pain from respiratory movements, exaggerated con-
sciousness of respiration (effort syndrome), hyperventilation syndrome,
secondary respiratory alkalosis (increased intracranial pressure, metabolic
acidosis).
Orthopnea–shortness of breath when lying down. This may occur as the
result of redistribution of extracellular uid from the periphery to the lungs,
an elevated diaphragm from obesity or ascites, or muscular weakness exacerbated by upward pressure of the abdomen on the diaphragm and thorax
when supine. Consciously or unconsciously, most patients with orthopnea
sleep and rest with their head and chest elevated, often in a seated position.
Estimate severity by the number of pillows required or if the patient sleeps
in a chair to achieve a comfortable sleeping position. Many patients also have
paroxysmal nocturnal dyspnea. Ask about orthopnea specically and observe
the patient for several minutes while supine.
Abnormal Alveoli—Alveolar Filling: Pulmonary edema, pulmonary
Compression of Alveoli: Atelectasis, pneumothorax, hydro-
Restrictive Chest and Lung Disease: Paralysis
Abnormal
Oxyhemoglobin Deciency: Anemia,
Paroxysmal nocturnal dyspnea. With recumbency, uid from edematous
extremities is redistributed to the vasculature and lungs increasing pulmonary capillary pressure (PCWP) and, in extreme cases, causing pulmonary
edema. Sudden paroxysms of breathlessness occur with recumbency, often
accompanied by orthopnea and coughing. Sitting or walking for a few minutes relieves the dyspnea. Airway disorders such as asthma may also result
in nocturnal dyspnea accompanied by sudden awakening, cough and wheezing. Unlike uid-redistribution related paroxysmal nocturnal dyspnea, these
patients do not typically have edema or preceding orthopnea and they may
improve rapidly with inhaled bronchodilators.
Platypnea–shortness of breath on standing. With standing, pulmonary
arteriovenous shunts may increase right-to-left shunting resulting in
decreased oxygen saturation (orthodeoxia) and shortness of breath.
is characteristic of the hepatopulmonary syndrome (see page 346) seen with
advanced liver disease. Patients complain of shortness of breath and
weakness on standing, relieved by sitting or lying. They have stigmata of
advanced liver disease including cutaneous spiders and ascites caused by
portal hypertension.
Platypnea
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