Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2853_Библиотеки_им_академика_М_И_Перельмана
.pdf
346 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
https://t.me/medicina_free
causing pulmonary inammation and/or hemorrhage and acute kidney in-
Goodpasture syndrome often presents acutely with dyspnea, hemop-
jury.
tysis, and cough. Granulomatosis with polyangiitis (Wegener) may be acute
or subacute. Limited forms of both occur. Prompt diagnosis and treatment is
required to preserve kidney function.
Sarcoidosis.
gans singly or in combination.
and mediastinal lymph nodes are most commonly affected. Patients may be
asymptomatic or present with nonproductive cough and dyspnea accompanied by fever, malaise, weight loss, and night sweats. Lung exam is normal or
shows crackles. Hepatosplenomegaly, lymphadenopathy, uveitis, cutaneous
plaques, and salivary gland enlargement are other manifestations.
Hepatopulmonary syndrome. Pulmonary arteriovenous shunts enlarge with
standing leading to decreased oxygen saturation (orthodeoxia) and shortness
of breath. The cause appears to be circulating vasodilators usually metabolized in the liver. Patients have advanced liver disease with portal hypertension and portosystemic shunting, with or without cirrhosis. They complain
of shortness of breath and weakness with standing and may become visibly
cyanotic when upright. Symptoms are often relieved by sitting and always by
lying down. Patients may become unable to sit or stand for any length of time.
Physical exam shows stigmata of chronic liver disease including spider angiomata and ascites. Diagnosis is by bubble contrast echocardiography showing
contrast in the left atrium in more than three but less than seven cardiac cycles.
Tracheal or bronchial obstruction. Complete obstruction of the trachea is
incompatible with life. Partial obstruction by a foreign body, neoplasm, or
other plug produces forceful prolonged inspiratory effort with retraction of
the intercostal spaces, suprasternal notch, supraclavicular fossae, and epigastrium. A low-pitched rhonchus or stridor, may be heard over the chest
and at the opened mouth during inspiration and expiration. In a ball-valve
obstruction the rhonchus occurs only during inspiration or expiration. An
isolated wheeze suggests a localized bronchial obstruction by bronchial adenoma, carcinoma, or foreign body. Bagpipe sign, another indication of partial
bronchial obstruction, is an expiratory sound persisting after a short a forced
expiration is abruptly stopped. If the obstructive rhonchus is heard on both
sides of the chest, the affected side is the one with the palpable rhonchus.
In obstruction of a large bronchus, trachea swings toward the affected side
during inspiration and away from it with expiration. A moving foreign body
can cause an audible slap with coughing or breathing. Slowly developing
bronchial obstruction may be asymptomatic, but sudden obstruction causes
severe dyspnea. Higher-pitched rhonchi arise from smaller bronchi. Causes
of large airway obstruction include aspirated foreign bodies, intraluminal
benign neoplasms (bronchial adenoma, amyloidoma), malignant neoplasm,
relapsing polychondritis, extrinsic compression from mediastinal masses
(retrosternal goiter, neoplasms, teratoma), laryngeal mass or paralysis, and
tracheomalacia following prolonged endotracheal intubation.
Noncaseating granulomatous inammation involves many or-
The cause is unknown. The lungs and hilar
Chronic obstructive pulmonary diseases. Expiratory airow obstruction
is the hallmark of asthma and chronic obstructive lung disease (COPD). In
Chest, Cardiovascular, and Respiratory Syndromes 347
https://t.me/medicina_free
asthma the obstruction is initially fully reversible and may be either xed or
partially reversible in COPD. Air trapping increases residual volume sustaining an inspiratory chest position (at diaphragm, horizontal ribs, increased
anterior–posterior diameter, hyperresonance) which increases the work of
breathing and decreases inspiratory capacity. The combination of history,
physical signs, chest radiographic features, and pulmonary function testing
allow differentiation.
Asthma.
ness to allergic and nonallergic stimuli resulting in airway inammation,
hyperplasia of mucous-producing goblet cells, and bronchial smooth muscle
hypertrophy. All of these features decrease airway diameter and airow resistance. Airow obstruction affects exhalation more signicantly secondary
to the decrease in airway size during normal exhalation. Airway obstruction
leads to air trapping and lung hyperination because of this differential effect on exhalation ows and exhaled lung volumes compared to inhalation.
Active disease may be subclinical and asymptomatic patients may have signicant airway inammation.
chest exam is normal. Asthma exacerbations begin with nonproductive cough
and progressive dyspnea. Nocturnal awaking with coughing and chest tightness is common. Sitting and leaning over a table or chair back improves the
dyspnea. The respiratory rate does not increase initially, but inspiration is
short while expiration is prolonged and labored. The patient is often anxious.
As air trapping attens the diaphragm, the chest becomes hyperresonant
maintaining an inspiratory position. During inspiration, the costal margins
diverge only slightly or converge. In severe asthma attacks, the sternocleidomastoid and platysma muscles tense and the alae nasi are with each inspiratory effort. Wheezing becomes less prominent as airway narrowing worsens.
Auscultation discloses decreased air movement, wheezes, and coarse crackles. Localized absence of breath sounds suggests bronchial plugging. As the
attack subsides, clear tenacious sputum is raised, and breathing gradually
becomes less labored. Asthma can occur without wheezing. The only sign
that consistently identies severe asthma exacerbation is use of the accessory
muscles of respiration. Severity is assessed by clinical history and bedside
or home airow measurements (Table 8-1). DDX: Wheezing occurs in acute
bronchitis, without the labored respiration. When wheezing is limited to a
single region, bronchial obstruction from foreign body or neoplasm must be
considered. The sudden occurrence of LV failure or MR may closely simulate
asthma with wheezes and crackles, and labored breathing may limit heart
auscultation. Vocal cord dysfunction (i.e., paradoxical closure of the cords
during inspiration) is suggested by wheezing that is loudest over the neck
and is diagnosed by examining the glottis during an attack. The symptoms
and signs of asthma are often relieved by inhaled bronchodilators. Spirometry conrms reversible airway obstruction.
Asthma is an acquired syndrome of increased airway responsive-
Between attacks, the patient is well, and the
Emphysema. Smoking, and rarely alpha-1 antitrypsin deciency, lead to de-
struction of alveolar walls with loss of alveolar surface area. Decreased elastic
recoil leads to expiratory collapse of terminal airways. Patients present with
progressive dyspnea over months to years, often accompanied by gradual
weight loss. At end-stage, patients often exhale against pursed lips, especially
with exertion, the chest is hyperresonant, breath sounds are decreased and
348 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
https://t.me/medicina_free
TABLE 8-1Asthma Clinical Severity Classification.
Symptoms
; Peak Expiratory
FEV
1
Asthma Severity Day Night
Mild intermittent 2 or less d/wk 2 or less nights/mo ≥80; <20%
Mild persistent >2 d/wk >2 nights/mo ≥80; 20%–30%
Moderate persistent Daily >1 night/wk 60%–79%; >30%
Severe persistent Continual Frequent <60%; >30%
TABLE 8-2Gold Criteria for COPD Severity.
Stage Severity FEV1 (% Predicted) FEV
I Mild ≥80 <0.7
II Moderate <80 <0.7
III Severe <50 <0.7
IV Very severe <30 or <50 with respiratory failure or right
heart failure
exhalation is prolonged, (page 311). Wheezes and crackles are uncommon unless infection supervenes. Physical ndings correlate poorly with the severity
of airow obstruction or abnormalities of gas exchange. Spirometry detects
early obstructive airways disease. Severity is assigned using the Gold system
(Table 8-2). Alpha-1 antitrypsin deciency also produces liver disease that can
dominate the presentation.
Flow Variability
<0.7
/FVC
1
Chronic bronchitis. Chronic inammation and secondary airway infection
results from chronic exposure to tobacco smoke or indoor air pollution such
as smoke from coal or wood-red cooking stoves. Airways obstruction is
prominent, and hypoxia is common. Patients with chronic bronchitis, with
or without bronchiectasis, present with chronic cough productive of purulent sputum and progressive dyspnea. The clinical diagnosis is established
when the cough is productive of sputum for over 3 months duration for two
consecutive years. The lungs have diminished breath sounds and prolonged
expiration and may have wheezing and inspiratory crackles. Physical ndings correlate poorly with the severity of airow obstruction or abnormalities
of gas exchange and spirometry is required to conrm the diagnosis.
Bronchiectasis. Severe acute or chronic pulmonary infections damage the
walls of small bronchi producing multiple chronically infected dilatations.
Presentation is cough with purulent sputum and occasional hemoptysis or
recurrent pneumonia. Sputum is copious and purulent. A resonant chest
with coarse basilar crackles suggests bronchiectasis. Clubbing may be present. Chronic infection with nontuberculous mycobacteria is common. Highresolution CT imaging is diagnostic.
Chest, Cardiovascular, and Respiratory Syndromes 349
https://t.me/medicina_free
Churg–Strauss disease. See page 363.
Lymphomatoid granulomatosis.
cal lymphocytoid, plasmacytoid, and reticuloendothelial cells invade tissues
and vessels. Nodules of varying size are found in the lungs, skin, kidneys,
and central nervous system, usually sparing the spleen, lymph nodes, and
bone marrow. In contrast to granulomatosis with polyangiitis (Wegener), the
lung is always involved while the upper respiratory tract is usually spared.
Transition to malignant lymphoma is common.
Cardiovascular Syndromes: Proper assessment of heart disease patients
requires identifying the etiology, anatomic abnormalities, and physiologic
disorders associated with the condition and the patient’s functional capacity.
For example, a formal diagnostic statement would be “rheumatic heart disease, inactive; mitral stenosis, right ventricular hypertrophy and dilatation,
pulmonary congestion; atrial brillation; functional class II.”
Etiology. Common etiologies are congenital (genetic and developmental), infectious, rheumatic, hypertensive, and ischemic.
Anatomy. List abnormalities of the aorta and pulmonary arteries, coronary
arteries, endocardium and valves, myocardium, and pericardium. Congenital
anatomic abnormalities are either cyanotic or noncyanotic (i.e., with or without signicant right-to-left shunt).
Physiology. List disturbances in cardiac rhythm and conduction, myocardial,
systolic or diastolic dysfunction, and clinical syndrome (e.g., anginal syndrome, CHF, cardiac tamponade).
Function. Two commonly used functional classication systems are:
New York Heart Association classication of angina or dyspnea:
Class I (No Incapacity). Although the patient has heart disease, the func-
tional capacity is not sufciently impaired to produce symptoms.
Class II (Slight Limitation). The patient is comfortable at rest and with
mild exertion. Symptoms occur only with more strenuous activity.
Class III (Incapacity with Slight Exertion). The patient is comfortable at rest,
but has dyspnea, fatigue, palpitation, or angina with slight exertion.
Class IV (Incapacity with Rest). The slightest exertion invariably produces
symptoms, and symptoms frequently occur at rest.
Canadian Cardiovascular Society for angina:
Class I. No angina with ordinary activity but angina occurs with strenu-
ous or rapid or prolonged exertion.
Class II. Slight limitation of ordinary activity (e.g., walking more
than two level blocks or climbing more than one ight of stairs at a normal
pace).
Class III. Marked limitation of ordinary activity (walking one to two
blocks on the level and climbing one ight of stairs).
Class IV. Inability to carry on any physical activity without angina;
angina may also be present at rest.
A variegated array of lymphatic cells, atypi-
Six-dermatome pain syndromes. See Six-Dermatome Pain, page 350.
350 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
https://t.me/medicina_free
Myocardial Ischemia Six-Dermatome Pain Syndromes
Angina pectoris.
cardial oxygen demand and supply. Oxygen delivery abnormalities are
simplied by rearranging the Fick equation: MVO
consumption) = (coronary blood ow) × (myocardial arteriovenous oxygen
difference). Because the arteriovenous oxygen difference is nearly maximal
at rest, inadequate oxygen delivery is usually caused by inadequate coronary
ow. Flow is directly proportional to the pressure gradient across the coronary bed (aortic diastolic minus coronary sinus pressure) and inversely proportional to resistance in the coronary arteries. Therefore, the most common
cause of impaired oxygen delivery is atherosclerotic coronary artery obstruction. Vasospasm induced by cold or exertion may be superimposed. Increased
myocardial oxygen demand is caused by increases in heart rate, myocardial
contractility, ventricular systolic pressure, and/or ventricular cavity radius,
regardless of a change in cardiac output or stroke volume.
Angina pectoris is a deep, steady pain or discomfort lasting 1–10 minutes
in the six-dermatome region often accompanied by shortness of breath, anxiety, and/or diaphoresis. It is classically precipitated by exercise or anxiety and
relieved by rest. Other precipitants are related to the cause of increased myocardial oxygen demand: examples of increased work are sinus tachycardia
and atrial or ventricular tachycardias; digitalis, other inotropic agents, and
anxiety increase contractility; hypertension and aortic stenosis increase systolic LV pressure; and, aortic regurgitation and systolic heart failure increase
LV radius. Stable angina is reproducible, does not occur at rest without provocation, and does not awaken the patient at night.
angina has several classic provocations. (1) Exertion. An important characteristic of exertional angina is the lag period before the pain begins, and the time
to subside with rest. Exertional pain without a lag period suggests another
etiology. (2) Postprandial. Exertion after a heavy meal is common. (3) Intense
emotion. Fear, anxiety, and sexual desire increase heart rate, blood pressure,
and contractility. (4) Cold. Peripheral vasoconstriction and increased blood
pressure and heart rate contributor. (5) Positive inotropic or chronotropic drug
effects. Caffeine, amphetamines, and cocaine increase the heart rate and blood
pressure. (6) Anemia. Oxygen delivery is reduced when the hemoglobin is
<10 g/dL.
each relieve an angina attack. Complete relief of pain or other discomfort in the
six-dermatome band after the administration of nitroglycerin is strongly suggestive of angina pectoris but is not diagnostic. The pain of esophageal spasm also
responds to nitroglycerin. If headache or ushing occurs without pain relief,
stable angina is unlikely. Quality: Angina is usually described as crushing,
aching, tightness, or pressure, frequently illustrated by clenching the st over
the sternum, the Levine sign. Region–Radiation: The pain occurs anywhere
in the six-dermatome band. It is often most intense behind the sternum or in
the precordium, radiating into the neck or throat, or down the medial aspect
of either arm. Ischemia in the right coronary artery distribution can radiate
to the interscapular region of the back. Less frequently, the pain is felt in the
spine or right shoulder and arm. The rare patient complains of pain exclusively in the limbs or neck without chest pain. Severity: Pain may be mild,
moderate, or severe, sometimes with a sense of impending death. Timing:
The pain is continuous, not eeting or lancinating, usually lasting from 1 to
10 minutes. Physical Signs: There may be no physical ndings. S4 can occur
Angina is caused by a temporary mismatch of myo-
(myocardial oxygen
2
PQRST–Provocation: Stable
Palliation: Rest, a warm environment, and nitroglycerin may
Chest, Cardiovascular, and Respiratory Syndromes 351
https://t.me/medicina_free
during angina because the ischemic ventricle is less compliant. An S3 appears
less often. An apical systolic mitral insufciency murmur suggests papillary
muscle ischemia. LV dyskinesia can cause a palpable precordial bulge or apical thrust.
DDX: Anginal attacks are transient, (typically <10 minutes), which
usually excludes MI, dissecting aneurysm, PE, and neoplasm. Atherosclerotic
CAD is the most common cause, but less common causes of reduced coronary
ow include vasculitis, aortic regurgitation, LV hypertrophy, anemia, and
hypoxemia. Pain with swallowing and a sensation of food sticking suggest
an esophageal source. The supine position often initiates gastroesophageal
reux pain. Pain from cholecystitis is often postprandial without concurrent
exertion. Epigastric and/or right upper quadrant tenderness support gallbladder disease. Walking induced pain in the shoulder girdle or spine and the
chest without a lag period suggests musculoskeletal pain. Angina is clinically
classied as follows:
Typical, or denite, angina. Substernal chest discomfort of characteristic
quality and duration is provoked by exertion or emotional stress and
relieved by rest or nitroglycerin.
Atypical, or probable, angina. This is dened as meeting two of the three
characteristics of denite angina.
Noncardiac chest pain. This meets one or none of the typical angina charac-
teristics.
Variant angina pectoris (Prinzmetal angina). Coronary artery spasm with
ST-segment elevation occurs with or without angiographically detectable coronary narrowing. The pain quality and location resemble classic
angina, but the pain occurs at rest and recurs in cycles, often at the same
time each day. ST-segments on ECG are transiently elevated during pain
suggesting myocardial injury. Pain is relieved promptly by nitroglycerin.
Migraine and Raynaud phenomenon occur more commonly in patients
with variant angina.
Unstable angina and MI. The endothelium overlying an atherosclerotic
coronary plaque may rupture exposing plaque contents to platelets and
procoagulants initiating a platelet plug and brin clot. Vasoconstrictor
substances are released resulting in intermittent or xed arterial obstruction. Severe prolonged ischemia leads to myocardial necrosis. Lesser
degrees of ischemia result in unstable angina syndromes and myocardial
hibernation (decreased contractile function without pain or necrosis).
Less common causes of acute coronary syndromes are coronary artery
embolism and vasculitis. The transition from severe ischemia to infarction is gradual and depends upon the collateral coronary ow to the
ischemic area, the contractile state of the myocardium, and the previous
history of that myocardium. Myocardium subjected to repeated ischemic
episodes, e.g., stable angina, is less susceptible to infarction.
Unstable angina. Patients present with new angina worsening in severity
(more easily provoked and/or more difcult to relieve), lasting >15 minutes,
occurring at rest and/or awakening the patient from sleep but without myocar-
dial necrosis. Untreated patients have substantial risk of acute MI.
The TIMI Risk Score is used to estimate risk for rapid evolution to acute
ST-elevation MI in patients with unstable angina and non-ST-elevation acute
352 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
https://t.me/medicina_free
MI. Give 1 point each for age ≥65 years, ≥3 traditional risk factors (CAD family history, hypertension, hypercholesterolemia, diabetes, current smoker),
known ≥50% coronary stenosis, ST-segment changes, ≥2 anginal episodes
in the preceding 24 hours, aspirin use in the last 7 days, and elevated CK or
troponin. Scores of 0–2 are low risk, 3–4 intermediate risk, and ≥5 high risk.
Acute MI. MI occurs most commonly from the early morning hours to midday. The pain onset is usually not induced by exertion, nor does it remit
with rest. The discomfort is identical to angina pectoris in quality, location,
intensity, and constancy, but it lasts from 20 minutes to several hours. In some
cases, the pain quickly increases to an intensity seldom experienced with angina; this may be sustained for hours, after which the pain subsides to a dull
ache that can last days. The patient often complains of shortness of breath
possibly related to increased LV end-diastolic pressure, depressed systolic
function, or mitral insufciency from papillary muscle dysfunction. Nausea
and vomiting are common, particularly with inferior wall infarction. A sympathetic response is triggered with sweating, pallor, and cold moist skin. The
heart rate may be slow, normal, or accelerated; similarly, blood pressure may
be low, normal, or quite elevated. An S4 may be heard and the heart sounds
are often muted. Crackles may appear at the lung bases. Life threatening cardiac rhythms can occur at any time. A pericardial friction rub appears in ~15%
>24 hours after onset of the MI. Occasional MIs are painless, the diagnosis
being suggested by the associated symptoms and signs. Large, uncompensated infarcts rapidly progress to cardiogenic shock and death characterized
by hypotension, hypoxemia, decreased mental status and anuria.
MI terminology is based on EKG interpretation. Presentation with
ST-elevations is an ST-elevation infarction (STEMI). Untreated, a STEMI
develops Q-waves, becoming a Q-wave MI. If a Q does not form, it is a non-
Q-wave MI. If no ST-elevation occurs, it is a non-ST-elevation MI (NSTEMI).
An NSTEMI usually does not form a Q-wave, so is a non-Q-wave MI. If a
Q-wave does appear, the NSTEMI is Q-wave infarction.
is excluded by the pain’s long duration and lack of response to rest and nitroglycerin. Three potentially life-threatening disorders closely mimic the pain
and presentation of MI: pulmonary embolism, (page 343), acute thoracic aorta
dissection (page 354), and acute pericarditis (page 352). PE is suggested by
clear lung elds and normal chest X-ray in the setting of marked dyspnea
and hypotension. Dissection pain is more excruciating and reaches its peak
more rapidly than MI pain. Prominent pain in the back makes dissection
more likely, however, pain radiating to the back occurs with MI and may be
absent with dissection. A new aortic diastolic murmur transmitting down the
right sternal border, and/or asymmetrical pulses or blood pressures between
extremities, suggests dissection, as does a widened superior mediastinum on
chest X-ray. The pain of acute pericarditis may be severe and resemble MI
though the pain may be intensied by reclining, breathing or swallowing.
That pericarditis can be a sequela of MI adds potential confusion.
DDX: Simple angina
Inammatory Six-Dermatome Pain Syndromes
Acute pericarditis.
etal pericardium are anesthetic (Fig. 8-44), but the outer surface of the lower
parietal pericardium is pain sensitive. The parietal pleura surrounds the
anterior and lateral pericardium, accounting for pleural involvement from
The visceral pericardium and inner surface of the pari-
Chest, Cardiovascular, and Respiratory Syndromes 353
Aorta
Phrenic nerves
https://t.me/medicina_free
FIG. 8-44 Pleuropericardial Relationships. A transverse section of the lower thorax with anesthetic serosal surfaces
represented by heavy beaded lines and pain-sensitive surfaces by lighter beaded lines. Note the proximity of the phrenic
nerves and esophagus to the parietal pericardium, so pericarditis can produce pain in the phrenic nerve distribution or pain
on swallowing.
pericarditis. Inammation can involve the closely positioned esophagus and
phrenic nerves causing dysphagia and phrenic pain. All these structures are
innervated by bers from the vagus and six-dermatome band. Phrenic nerve
sensory bers from the central diaphragm can be irritated in the lower pericardium causing neck pain at the superior border of the trapezius.
toms: Deep constant or pleuritic pain occurs in the six-dermatome band or
the phrenic distribution. The location and quality of pain often resembles that
of MI, but it is usually accentuated by breathing or coughing, worse in recumbency, and lessened while sitting and leaning forward. It may be intensied
by swallowing. Pleuritic pain referred to the shoulder, particularly the left
trapezius ridge, suggests pericarditis (Fig. 8-43, page 340). The pain may last
for hours and is not relieved by nitroglycerin. Rarely, the pain is throbbing
and synchronous with the heartbeat.
pain. A transient pericardial friction rub is often heard.
elevation followed by T wave inversion is diagnostic. The ST-T ndings of
pericarditis must be differentiated from the injury currents of infarction and
normal early repolarization. DDX: Causes of pericarditis include infection,
malignancy, rheumatic fever, collagen vascular diseases, trauma, uremia, or
following MI or chest radiation. Until a pericardial friction rub appears or
ECG signs develop, the steady pain suggests MI, dissecting aneurysm, pulmonary infarction, cholecystitis, or peptic ulcer. Pain on swallowing can suggest an esophageal lesion. The pleural pain must be distinguished from that
of pleurisy, subphrenic abscess, and splenic infarction.
Post-cardiotomy syndrome. A hypersensitivity reaction to antigen derived
from injured myocardium occurs several weeks after MI, cardiac surgery, or
other heart injury. Findings are fever, pericarditis, pleuritis, pericardial and/
or pleural effusions, and pneumonitis. Recurrences are common, usually with
decreasing severity. The symptoms often respond dramatically to NSAIDs.
Recurrent MI should be considered in patients with ischemic heart disease.
The appearance of a pericardial friction rub, and absence of new Q-waves or
Esophagus
Lung
Visceral
pericardium
Parietal
pericardium
Lung
Parietal pleura
Visceral pleura
Heart
Sternum
Symp-
Signs: Fever may follow the onset of
ECG: Widespread ST
354 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
https://t.me/medicina_free
ST-segment depressions on ECG help distinguish post-cardiotomy (Dressler)
syndrome from recurrent MI.
Mediastinal and Vascular Six-Dermatome Pain Syndromes
Aortic dissection. Cystic medial necrosis and intramural hemorrhage
lead to intimal rupture, or the intimal tear can be the primary event. The
intimal tear occurs most commonly in the lateral wall of the proximal
ascending aorta, or, less commonly, just distal to the ligamentum arterio-
sum in the descending aorta. Luminal blood penetrating the weakened
media produces a hematoma that splits the vessel wall. Distal progres-
sion sequentially occludes aortic branches causing distal ischemia. A
second intimal tear may occur distally providing egress from the false
lumen creating a double-barreled aorta.
branches of the aorta, accompanied by loss of specic nerve functions.
Symptoms: In 80% of cases, the onset is sudden, with excruciating pain
in the precordium and/or the interscapular region that moves succes-
sively to the lower back, abdomen, hips, and thighs. The pain often sug-
gests MI. Sometimes the onset is gradual without chest pain.
pressure is usually unaffected. Cardiogenic or hemorrhagic shock may
occur with rupture into the pericardium or left pleural space respectively.
Proximal Progression: A hematoma extending proximally from a tear in
the aortic arch can distort the aortic valve ring separating the commis-
sures to cause aortic regurgitation and a murmur transmitting down the
right sternal border, occlude the coronary ostia causing an MI, produce
hemopericardium with a pericardial rub and cardiac tamponade, and/
or swell the base of the aorta pulsating the sternoclavicular joint.
tal Progression: When the hematoma extends away from the heart there
is sequential asymmetrical decrease or loss of pulses in branches of the
aorta and signs of nervous system injury. Carotid occlusion causes cere-
bral ischemia with localizing neurologic signs. Obstruction of the spinal
arteries is indicated by paraplegia and anesthesia. Renal artery occlu-
sion with infarction causes pain simulating renal colic. Aortic dissection
may be rapidly fatal. Chest X-ray: Widening of the aorta, an enlarged
aortic knob, or separation of calcied intimal plaques from the outer
border of the aortic wall all suggest dissection. Imaging studies should
be performed urgently when dissection is suspected.
monly, dissection occurs in association with cystic medial necrosis of the
aorta, especially in patients with Marfan and Ehlers–Danlos syndromes.
It occurs with less frequency in patients with hypertension, advancing
age, during labor, and after penetrating or blunt trauma. Dissection may
occur in a thoracic aortic aneurysm aficted with aortitis from bacteria,
syphilis, or giant cell arteritis.
Leakage and rupture of aortic aneurysm. Expanding aneurysms are usu-
ally painless, but breach of the wall with leakage of blood into the sur-
rounding tissue is accompanied by the sudden severe pain at the site of
leakage or radiating into the body wall at that spinal segment. The pain
is often accompanied by restlessness, diaphoresis, and tachycardia. The
specic pain pattern reects the site of leakage. Urgent evaluation and
intervention required to prevent death. Complete rupture presents as
Pulses are progressively lost in
Signs: Blood
Dis-
DDX: Most com-
Chest, Cardiovascular, and Respiratory Syndromes 355
https://t.me/medicina_free
sudden severe pain followed shortly by death from rapidly progressive
hemorrhagic shock.
Spontaneous esophageal rupture—Boerhaave syndrome. Forceful vomiting precipitates chest or upper abdominal pain and severe dyspnea.
Subcutaneous emphysema can dissect into the supraclavicular fossae
accompanied by a precordial crunching sound from mediastinal emphysema (Hamman sign). DDX: The symptoms are common to MI, perforated
peptic ulcer, cholecystitis, pancreatitis, esophagitis, hepatitis, nonperforating ulcer, and pneumonia. Radiographic demonstration of air in the
mediastinum excludes all the foregoing in favor of ruptured esophagus.
Six-dermatome pain with dysphagia. See Chapter 9, page 432.
Subphrenic diseases. Lesions below the diaphragm usually present with ab-
dominal pain, but there are frequent exceptions so consider subphrenic disorders with six-dermatome band pain. Subphrenic abscess, acute cholecystitis,
peptic ulcer, acute pancreatitis, and splenic infarction are considerations.
Pulmonary artery embolism and pulmonary infarction. See page 343.
Pneumothorax. See page 340.
Other Cardiovascular Syndromes
Pulmonary edema. See page 344.
Cardiac dilatation.
Dilatation of heart chambers is caused by poor systolic
function or chronic volume overload. The dilated heart of trained athletes has a
large stroke volume that maintains high cardiac output at relatively low heart
rates, thereby minimizing myocardial oxygen demand. Heart enlargement,
indicated by displaced apical impulse and borders of cardiac dullness or chest
radiograph, implies dilatation of one or both ventricles. When the dilated heart
also has depressed contractility, the elongated myocardial muscle bers generate weak and often diffuse apical impulses. An apical impulse displaced leftward with a normal right heart border suggests LV dilation.
effusions will enlarge the heart silhouette and borders of dullness, but the apical impulse is usually undetectable, and the heart sounds are diminished.
CLINICAL OCCURRENCE: Left Ventricular Dilation: Aortic insufciency,
mitral insufciency, ischemic cardiomyopathy, post-MI, dilated cardiomyopathy, viral myocarditis;
Right Ventricular Dilation: Pulmonic insufciency,
tricuspid insufciency, ASD with left-to-right shunt, right ventricular infarct,
pulmonary hypertension with RV failure.
Myocardial hypertrophy. Hypertrophy, with or without dilation, is the
result of pressure and/or volume overload or hypertrophic cardiomyopathy.
Hypertrophied LV myocardium produces more powerful apical impulses
than normal. The heart is not enlarged on physical exam without concomitant
dilation (Fig. 8-45). Right ventricular hypertrophy can produce a palpable
thrust over the right ventricle along the left sternal edge.
CLINICAL OCCURRENCE: LV Hypertrophy: Valvular aortic stenosis, mitral
or aortic insufciency, hypertension, hypertrophic cardiomyopathy; Right
DDX: Pericardial
Соседние файлы в папке Библиотека им академика М.И. Перельмана