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366 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
Ster
oid bone
tilage
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Temporal a.
Internal carotid a.
External carotid a.
nocleidomastoid m.
Carotid sinus
Common carotid a.
Clavicle
Right subclavian a.
FIG. 8-47 Large Superficial Arteries of the Head and Neck. The accessible arterial segments are diagrammed in
solid black; inaccessible parts are stippled. The temporal artery courses anterior to the ear and upward to the temporal
bone. The carotid arteries are deep to the anterior margin of the sternocleidomastoid muscle. The carotid sinus, at the
bifur cation of the c ommon caroti d, is level with t he upper margi n of the thyroi d cartilag e. A short segme nt of the subclavian
artery is often palpable in the supraclavicular fossa.
Hy
Thyroid car
FIG. 8-48 The Aortic Arch. A. Aortic arch variations. The normal pattern is only slightly more common than the
other t wo. 1. The normal pattern has a right innominate artery, branching into the subclavian and common carotid. There
is no left innominate artery, the left subclavian and common carotid originating from the aorta itself. 2. There is both a
right and left innominate. 3. The right innominate gives off the left common carotid in a ddition to th e right
carotid and subclavian. B. Anatomic relations of a dilated aortic arch. Aneur ysm of the aortic arch or dilatation of the
left atrium may compress the left recurrent laryngeal nerve against the vertebrae or the left main bronchus producing paralysis
of the left vocal cord, resulting in hoarseness or a brassy cough. Expanding downward, the arch impinges upon the left main
bronchus depressing the trachea with each pulse wave, giving a physical sign called the tracheal tug.
a substantial risk for stroke within hours or days. Bruits without symptoms
must be evaluated to assess the severity of obstruction.
Vertebral artery disease. The vertebral arteries are not accessible to direct
examination. They join to form the basilar artery in the posterior fossa and
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collateralize the cerebral circulation via the posterior cerebral and posterior
communicating arteries. Vertebral occlusive disease occurs because of atherosclerosis or dissection giving symptoms of brainstem ischemia (e.g., vertigo,
dysarthria, dysequilibrium).
Arterial Aneurysms. Aneurysmal arterial dilatation may be congenital or
result from cystic medial necrosis, atherosclerosis, hypertension, vasculitis, or
infection. Aneurysms are fusiform, saccular, or dissecting. They may consume
platelets and clotting factors. Similar physical signs are produced by fusiform
and saccular dilatations, but the arterial dissection presents an entirely different clinical picture (aortic dissection, page 354). Pain accompanying an
aneurysm suggests a penetrating aortic ulcer, leakage, or dissection of the
arterial wall.
Thoracic aneurysms.
Breakdown of structural proteins in the aortic media and adventitia leads to
smooth muscle necrosis and development of cystic spaces lled with mucoid
material (cystic medial necrosis). Predisposing factors include genetic abnormalities (e.g., Marfan syndrome), hypertension, pregnancy, inammation
(e.g., GCA, syphilis), and possibly atherosclerosis.
classied by their proximal extent, regardless of distal extension, into those
involving the ascending aorta and those only involving the aorta distal to the
left subclavian artery. The signs and symptoms are due to compression or distortion of adjacent structures and pain from medial dissection or sudden dilation without dissection. Dissection can occur prior to aneurysmal dilatation.
Ascending aortic aneurysms. These can produce aortic regurgitation from
either dilation of the ascending aorta or proximal dissection extending
to the valve ring and leaets. The murmur characteristically transmits down
the right sternal border rather than the left. A palpable thrust may develop
in the right second or third intercostal spaces. The width of manubrial dullness is increased. Erosion of ribs and protrusion of a pulsatile mass can occur.
Compression signs include hoarseness (recurrent laryngeal nerve traction),
cough, wheezing, or hemoptysis (compression and/or erosion of bronchi).
Acute six-dermatome chest pain may result from dissection or myocardial
ischemia from dissection of coronary ostia (usually the right). Proximal dissection can rupture into the pericardium producing acute tamponade.
Aortic arch aneurysms. Retrosternal pain is frequent, radiating to the left
scapula, left shoulder, or left neck. The dilated arch can compress the left recurrent laryngeal nerve against the trachea or the left main bronchus causing
hoarseness and a brassy cough (Fig. 8-48B). Obstruction or dissection of the
left subclavian artery causes delay and diminution of pulse volume and reduces left arm blood pressure by >20 mm. The dilated aortic arch can depress
the left main bronchus producing a tracheal tug with each beat detected by
grasping the cricoid cartilage lightly with the thumb and forenger feeling
the trachea dip with each pulse (Fig. 8-48B).
The cause of thoracic aneurysms is multifactorial.
Thoracic aneurysms are
Descending aortic aneurysms. These are frequently silent and discovered
incidentally. They may erode vertebral bodies causing back pain radiating
around the chest via the intercostal nerves. Dissection can occlude spinal
368 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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arteries producing paraplegia. Pain from dissection of descending thoracic
aneurysms is like pain from acute MI or ascending aorta dissection, except
that the most have pain in the back with or without anterior chest pain.
Abdominal aortic aneurysm (AAA). These are the most common aortic
aneurysms. AAA involves all three layers of the aorta. The risk of rupture is
directly related to its diameter. Aortic atherosclerosis is uniformly present and
often widespread.
prevalence increases with each decade. Major risk factors are atherosclerosis, cigarette smoking, and male sex. Family clustering has been noted. The
width is estimated by placing the ngers on the lateral walls of the pulsatile
mass just cephalad to the umbilicus. Pulsatile expansion is demonstrated by
lateral as well as anteroposterior movement; this does not occur with a solid
mass anterior to the aorta transmitting pulsations. Imaging is required for
reliable measurement of size and changes over time. The presence or absence
of abdominal or femoral bruits has no predictive value for the presence or
absence of AAA. Pain in the mid to lower abdomen and the appearance
of a pulsatile epigastric mass suggest recent expansion or leaking. Rapid
enlargement in size may, however, be asymptomatic. Rupture is associated
with severe pain in the abdomen, back, and/or inguinal areas, accompanied
by hypotension. The sensitivity of abdominal palpation for the detection of
AAA depends upon the size of the aneurysm and the patient’s body habitus.
Aneurysms >5 cm in diameter are at risk of rupturing and should be considered for elective surgery. Physical exam is only 75% sensitive for detecting
aneurysms of this size. Diagnostic imaging is the preferred method of detection, and male smokers between 65 and 75 years of age are considered for
screening. Iliac artery aneurysms, felt on deep palpation as pulsatile masses
in the lower abdominal quadrants, are not rare and may rupture.
AAA is uncommon in individuals younger than age 60, but
Dissecting aortic aneurysm. See page 354.
Mycotic aneurysms. These saccular aneurysms are the result of a weakened
arterial wall resulting from infection, most frequently an embolic arteritis
resulting from subacute bacterial endocarditis or septicemia. They can also
develop as extensions of localized suppuration, actinomycosis, or tuberculosis. Mycotic aneurysms usually develop in vessels subject to bending and
lightly protected by overlying muscles, e.g., the axillary, brachial, femoral,
and popliteal arteries.
Coarctation of the aorta. A congenital stricture forms just proximal or distal
to the aortic insertion of the ductus arteriosus (preductal or postductal). The
most common constriction is distal to the left subclavian artery takeoff. The
adult type almost invariably has a closed ductus. Tissue perfusion distal to
the coarctation is maintained via high resistance chest wall collaterals perfusing at the expense of sustained central arterial hypertension. The collateral arterial circulation is via the left internal mammary artery and other left
subclavian branches, to the left intercostal arteries (excepting the rst two),
the musculophrenic, and the superior epigastric arteries (Fig. 8-49). In most
cases the collateral circulation allows the patient to remain asymptomatic
into adulthood. There is hypertension in the arms with slight hypotension
and a dampened pulse wave in the legs. A coincident bicuspid aortic valve
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FIG. 8-49 Coarctation of the Aorta: Collateral Circulation. The diagram shows the collateral channels from the
costocervical trunk and the internal mammary artery causing dilatation of the intercostal arteries. The circulation around the
scapula is augmented by blood through the transverse cervical artery. The pulse volume in the arms is normal; in the femoral
arteries it is diminished. The dilated scapular and intercostal arteries may be palpable in the back.
is common, so aortic systolic and/or diastolic murmurs may be heard. The
Murmur: The murmur of the coarctation is heard best in the posterior inter-
scapular area. The site of constriction is remote from the precordium, so the
murmur is faint, if heard at all, on the anterior chest. When a murmur is audible anteriorly, it is usually a brief early systolic ejection murmur caused by an
associated bicuspid aortic valve, often with an early systolic ejection sound.
A continuous bruit from the dilated internal mammary arteries is sometimes
heard over the sternum. Arterial Pulses: The dampened pulse wave in the
distal aorta and its branches is most easily detected by palpating the femoral arteries. When the femoral pulses have good volume, a peak pulse lag
between the radial and femoral arteries suggests coarctation. Palpable collateral circulation through the dilated intercostal arteries in the posterior intercostal spaces is diagnostic. Notching of the inferior rib margins posteriorly is
visible on chest X-ray. Hypertension in young adults suggests the possibility
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FIG. 8-50 Two Syndromes of Large Artery Obstruction. A. Obstruction at the aortic bifurcation (Leri-
che syndrome): a short thrombus closes the lower part of the abdominal aorta and extends a variable distance down the
common iliac arteries. The accessible segments of the femoral, popliteal, dorsalis pedis, and posterior tibial arteries are pulseless. Pain in the legs and intermittent claudication are the common symptoms. B. Subclavian steal syndrome: the most
common site of narrowing is the left subclavian artery, although other sites have also been reported.
of coarctation. Coarctation is common in patients with the gonadal dysgenesis (Turner syndrome).
Aberrant right subclavian artery (dysphagia lusoria). Chapter 7, page 252.
Subclavian steal syndrome. Atherosclerotic subclavian artery stenosis
proximal to the vertebral artery origin results in retrograde ow in the ipsilateral vertebral artery inducing brainstem ischemia with neurologic signs
(Fig. 8-50). A bruit may be heard in the supraclavicular fossa, occasionally
with a thrill. The arterial pulse volume and blood pressure are diminished in
the affected arm. Symptoms and signs of cerebral ischemia are intermittent or
continuous, ranging from vague dizziness to vertigo, slurring of speech, and
hemiparesis. The neurologic signs and symptoms can be induced by exercising the affected arm.
Thoracic outlet syndromes—subclavian and brachial plexus compression.
The roots of C5-T1 form the brachial plexus in the lateral neck between the
scalenus medius and the scalenus anticus. The subclavian artery exits the rib
cage over the rst rib. Artery and nerves run together over the rst and second
ribs and under the clavicle and pectoralis minor into the upper arm. These
syndromes are caused by compression of the nerves and vessels coursing
between muscles and bones while making their exit from the neck (nerves)
and chest (vessels) (
pression, are largely sensory (paresthesias), and signs are those of positional
arterial obstruction. Examine a patient presenting with subjective neurologic
symptoms for signs of arterial compression.
Scalenus anticus syndrome. There is intermittent or constant pain and/or
paresthesia in the ulnar aspect of the arm and hand, sometimes associated
with weakness and wasting. Adson Test, Fig. 8-51a: Have the patient sit with
the palms on the knees, chin high, and turned to the side being examined.
Examine the radial pulse with breath holding in deep inspiration. A positive
Fig. 8-51). Symptoms, arising from brachial plexus com-
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FIG. 8-51 Compression Syndromes of the Superior Thoracic Aperture. A. Scalenus anticus syndrome:
the scalenus anticus muscle attaches to the transverse processes of the cervical vertebrae above and below to the first rib.
Posteriorly and behind the subclavian artery, the scalenus medius attaches to the same bones. Hypertrophy of the bellies of
the two muscles compresses the artery between them with motions such as turning the head to the ipsilateral side. This is
tested by the Adson maneuver (a), where the patient sits with chin raised, head rotated to the left, and chest held in
the inspiratory position. A positive test is marked by diminution or disappearance of the left radial pulse. The other side is
tested similarly. B. Cervical rib syndrome: th e diagram shows a cervical rib compressing the left scalenus anticus muscle
and indirectly the subclavian artery. This may diminish the radial pulse and/or produce a partial brachial plexus peripheral
neuritis. C. Costoclavicular syndrome: the geometry of the aperture may be such that rotating the clavicles downward
and back ward compresses the subclavian arterie s against the first rib. This is teste d (c) by having the pat ient seated in a chair
and the examiner standing behind him pushing the shoulders downward and backward while an assistant feels for diminution
of the radial pulses. D. Hyperelevation of the arm: in some persons thoracic geometry is such that hyperelevation
of the arm causes the coracoid process to impinge on and compress the subclavian artery, diminishing the radial pulse (d).
test is dampening or obliteration of the radial pulse that resolves when the
chin turns forward, still holding the breath. The syndrome is associated with
muscular hypertrophy or edema after unusually vigorous arm use or with
unusual occupations, such as weight lifters. Muscle spasm can result from
poor posture, anomalous rst rib, or cervical rib.
Cervical rib. In addition to producing scalenus anticus spasm (scalenus
anticus syndrome, above), a cervical rib can directly compress the subclavian
artery dampening the radial pulse in any position (Fig. 8-51B). Occasionally,
the extra rib is palpable in the supraclavicular fossa. The rib may also
compress the brachial plexus producing pain or paresthesias in the hand.
372 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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Costoclavicular syndrome. There is intermittent or constant pain and/or paresthesia in the ulnar aspect of the arm and hand. Have the patient stand with
arms at the sides and elbows exed at 90 degrees. Then elevate the elbows to
45 degrees, 90 degrees, and 135 degrees (this last position puts the hands on
the head). Palpate the radial pulse and auscultate beneath the mid-clavicle
at each position. Patients with costoclavicular syndrome obliterate the pulse
in at least one position. A palpable pulse with a subclavicular systolic bruit
indicates partial obstruction. Costoclavicular Maneuver: This test for clavicular
compression of the subclavian artery on the rst rib is specic but not sensitive. The patient sits, an assistant palpating his radial pulses. Standing behind
the patient force his shoulders down and back narrowing the thoracic outlet
(Fig. 8-51C and c). Compression sufcient to cause symptoms, diminishes the
pulse volumes. Activities in which the shoulders are forced downward and
backward, such as walking with a heavy backpack carried on the shoulders
are often the cause.
Ischemia from arm elevation. In some persons, arm elevation compresses the
subclavian artery on the coracoid process (Fig. 8-51D and d). The patient complains of intermittent or constant numbness and tingling in one or both hands
or arms. Patients often sleep on their back with the hands behind or over the
head. Another precipitant is working with the arms elevated, such as painting
ceilings. Hyperabduction Test: Have the patient lift the hand to the top of the
head then open and close his hand several times noting whether the radial
pulse is diminished or abolished.
Superior vena cava (SVC) syndrome. The principal signs are edema and cyanosis of the head, neck, and both arms, edema of the face, both arms, and the
upper third of the thoracic wall, and engorged venous without the pulsations
normally transmitted from the right atrium (Fig. 8-52). The neck is enlarged
by nonpitting edema (Stokes collar) and collateral veins may be visible on
the chest and abdominal wall. Causes are mediastinal neoplasm, cervical or
retrosternal goiter, thoracic aortic aneurysm, chronic mediastinitis (e.g., histoplasmosis), thrombosis from an indwelling intravenous catheter.
Inferior vena cava (IVC) obstruction.
age from the legs and pelvis leading to development of collateral veins in the
hemorrhoidal complex and abdominal wall. Renal vein thrombosis causes
acute renal failure.
lower extremity edema develops. Symmetrical rapidly progressive edema
of both legs without evidence of heart or kidney disease suggests mechanical IVC obstruction. Chronic IVC Obstruction: Dilated supercial collateral
veins with cephalad ow on the abdomen suggest chronic IVC obstruction.
Visible collaterals can appear within a week of obstruction, the veins attaining
maximal size in 3 months. To localize the obstruction, consider the vena cava
in three segments (Fig. 8-52). Lower Segment (below the renal veins): The
collaterals are distributed over thighs, groins, lower abdomen, and anks.
Leg edema, initially pitting, develops brosis with chronic venous stasis dermatitis. Pelvic congestion produces low back pain and genital edema. Middle
Segment (above the renal veins and below the hepatic vein): The venous col-
laterals are large intra-abdominal veins without abdominal wall collaterals.
Occlusion of the renal veins produces nephrotic syndrome. Gastrointestinal
Acute IVC Obstruction: It may be asymptomatic until
IVC occlusion impairs venous drain-
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FIG. 8-52 Superior and Inferior Venae Cavae.
manifestations include nausea, vomiting, diarrhea, and abdominal pain.
Malabsorption may develop. Upper Segment (above the hepatic veins):
Venous collaterals form a prominent periumbilical plexus and large veins
appear over the anterior abdomen. Budd–Chiari syndrome develops with hepatosplenomegaly, ascites, jaundice, and elevated transaminases.
CLINICAL OCCURRENCE: Intraluminal: Thrombosis, embolism, invading
neoplasm, or extension from renal cell carcinoma; Intramural: Rare benign or
malignant neoplasms; External Pressure: Hepatomegaly, lymphadenopathy,
aortic aneurysm, surgical ligation, and pregnancy.
Disorders of Large Limb Arteries. Arterial disorders are occlusive or nonocclusive, and occlusion may be partial or complete. Four mechanisms cause
arterial circulatory decits: (1) extrinsic compression; (2) vasospasm; (3) luminal obstruction (intimal thickening, thrombus, embolus); or (4) arteriopathy
(vasculitis, bromuscular dysplasia). Temporary arterial compression is often
related to extremity positioning. Vasospasm is recognized by the sharp border between ischemic and normal tissue. Intimal proliferation is inferred
when the blood ow is diminished but still present. Complete occlusion is
usually caused by embolism or thrombosis. Thrombosis is often the result of
gradual, usually atherosclerotic, narrowing allowing development of collaterals with relatively mild symptoms coming on gradually. Sudden embolic or
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thrombotic occlusion causes severe pain and a cold white part. Arteriopathy
such as vasculitis is usually inferred from the total clinical picture. When an
acute arterial occlusion is suspected, determine the most distal site with adequate ow by noting the presence or absence of pulses along the vessel and
palpate the vessel walls for signs of intrinsic disease. Urgent vascular imaging
is required by Doppler ultrasound, and/or CT, MR, or contrast angiography.
Atherosclerosis.
Atherosclerosis is characterized by degeneration and brosis
of the media together with occlusive intimal proliferation. Arterial narrowing
is the result of progressive intimal thickening, plaque formation with accumulation of cholesterol-rich lipid deposits, foam cells, and smooth muscle proliferation. Rupture of intimal plaques leads to thrombus formation. Arterial
segments lengthen and, when the ends of a segment are anchored, the elongated vessel buckles producing visible and palpable tortuosity. Atherosclerosis
may be diffuse or focal, often occurring at arterial bifurcations.
In patients
age >45, atherosclerosis is the major cause of arterial obstruction. Patients
with diabetes mellitus have an increased risk inversely related to glycemic
control. Hyperhomocysteinemia, congenital or acquired (folic acid and B
deciency), also increases risk for atherosclerosis and thromboembolic events.
12
Atheromatous plaques may be felt in the walls of accessible arteries, the vessels feeling thick and noncompressible. Noninvasive vascular examination
with Doppler ultrasonography and plethysmography are required for accurate diagnosis. Angiography with contrast or MRA is anatomically denitive.
Acute arterial obstruction. Occlusion of arteries to the organs of the head,
thorax, and abdomen presents with symptoms referable to those organs, e.g.,
stroke, acute MI, PE, mesenteric, renal, and splenic infarction.
Acute extremity artery obstruction—embolism and arterial thrombosis. This
is most common in the legs but does occur in the arms. The patient experiences sudden excruciating pain followed by numbness and weakness.
Occasionally, anesthesia and weakness are presenting symptoms while the
pain appears gradually. The distal extremity is pulseless and becomes pallid,
the skin becoming cool. Venous pooling causes the skin distally to gradually
become cyanotic while mottling occurs proximally; the cyanosis diminishes
with limb elevation. Occasionally, the pain may be quite mild. Thrombosis
is more likely when there are signs of diffuse vascular disease or a history of
claudication. Embolism is likely with atrial brillation.
CLINICAL OCCURRENCE: Thrombosis: Atherosclerosis, thromboangiitis
obliterans, vasculitis, infection, trauma, antiphospholipid syndrome, and
sludging from polycythemia, hemoconcentration, cryoglobulinemia, or
hyperglobulinemia; Embolism: Atrial brillation, mitral stenosis, endocarditis (infectious, NBTE), left atrial myxoma, LV mural thrombus post MI, and
atheroembolism.
Chronic peripheral vascular disease (PVD). PVD is most common in the
legs but can involve the arms. The patient complains of claudication and
coldness progressing to continuous and/or night pain. Measure the ABI
(page 291). Arterial insufciency causes skin pigmentation, pallor, purplish
discoloration fading with elevation, coldness, warm areas of collateral circulation, local hair loss, malnutrition of toenails, ulceration, and/or gangrene
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(Figs. 8-24 and 8-53). Pulses are weak or absent and muscle wasting may be
evident. Popliteal artery occlusion leads to collateral circulation via geniculate artery branches producing cold feet with especially warm knees or
anteromedial lower thigh. ABI of <0.9 is associated with increased risk of
cardiovascular morbidity and mortality. ABI <0.5 is more strongly associated
with decreased physical activity than with claudication.
Pulseless femoral artery. When examining the abdomen, always palpate the
femoral arteries. When a femoral pulse is diminished or absent, palpate the
iliac pulses up to and including the aortic bifurcation located 2 cm below and
slightly to the left of the umbilicus. The iliac arteries run in a line between
the bifurcation and the midpoint of the inguinal ligament. The upper third is
the common iliac, the lower two-thirds the external iliacs. Though these vessels may not be palpable in normal persons, nding asymmetry is signicant.
Bilateral decreased or absent femoral pulses suggest coarctation of the aorta,
distal aortic thrombosis (Leriche syndrome, Fig. 8-50A, page 370), or dissecting
aortic aneurysm. Unilateral absence suggests common iliac artery thrombosis. The signicance of an absent or diminished femoral pulse is determined
by the status of the distal pulses.
Thromboangiitis obliterans (Buerger disease).
mental panarteritis involving all three layers of medium-sized arteries,
intimal granulation tissue ultimately causes arterial obstruction, producing
tissue ischemia and necrosis. Thromboangiitis affects young male smokers
and is often associated with supercial migrating thrombophlebitis. It usually presents between ages 20 and 40, a younger age than atherosclerosis.
DDX: No physical signs distinguish Buerger disease from atherosclerosis.
The distribution of affected vessels may differ from atherosclerosis, thromboangiitis having a predilection for the radial, ulnar, and digital arteries, in
addition to affecting the lower extremities. Approximately 7% of Japanese
patients are nonsmokers.
Raynaud disease and phenomenon. Intense spasm of the digital arteries
and dermal vessels produces initial pallor, followed over minutes by lling
of dilated cappillaries with deoxygenated venous blood producing cyanosis.
Relaxation of arterial spasm ushes the capillaries with arterial blood producing the warm red phase of vasodilation. Approximately 80% of patients
are young women. The sudden attacks are induced by cold exposure or
emotional stress and last up to 60 minutes. Manifestations are unilateral or
bilateral, most commonly in the ngers, though the toes are affected in 50%
of cases. One to four ngers are involved, but rarely the thumbs. The terminal digits become chalk-white, numb and sweaty; intense cyanosis and pain
succeeds the pallor. Sometimes either pallor or cyanosis is absent. During
spontaneous recovery, or after warm water immersion, projections of
hyperemia replace cyanosis until the digit becomes brilliant red. Hyperemia
is accompanied by tingling, throbbing, and edema. After many attacks, trophic changes may appear in the nails and adjacent skin and small areas of
gangrene may develop on the ngertips and toes. The term Raynaud dis-
ease is used when there is no associated condition and Raynaud phenomenon
when it is associated with scleroderma, vibratory trauma, SLE, polyarteri-
Beginning as an acute seg-
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