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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
.pdf
USMLE Step 2 CK
l Internal Medicine
Table 5-9. Differential Diagnosis of Aortic Valve Stenosis
Disease Entity Differentiating Features
Aortic valve sclerosis of the
elderly, without stenosis
Hypertrophic obstructive
cardiomyopathy
Mitral regurgitation Murmur is holosystolic and radiates to axilla and not
Pulmonic stenosis Murmur does not radiate into neck; loudest along the left
Systolic murmur does not peak late
Carotids do not have delayed upstrokes
No left ventricular hypertrophy by EKG
Echocardiographic visualization of excursion of valve
leaflets usually normal or mildly reduced, but valves may
not be visualized
No hemodynamically significant aortic valve gradient by
cardiac catheterization
Brisk bifid carotid upstrokes
Murmur usually does not radiate into neck
Characteristic change in murmur with various maneuvers
Pseudoinfarct pattern (large septal Q waves) on EKG
Characteristic echocardiographic features
carotids
Carotid upstroke may be normal
Dilated left ventricle
Aortic valve normal on echocardiogram unless there is
associated aortic valve disease
sternal border; increases with inspiration
Physical examination, chest x-ray, and EKG may reveal
enlarged right ventricle
Echocardiogram reveals right ventricular enlargement and
hypertrophy
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Note: All of the above have a systolic murmur that can be confused with aortic stenosis.
Table 5-10. Effect of Various Maneuvers on Systolic Murmurs
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Chapter 5
l Cardiology
Aortic
stenosis
Hypertrophic
obstructive
cardiomyopathy
Ventricular
septal defect
Mitral
regurgitation
Phenylephrine
Valsalva
Decrease Decrease Increase or
Increase Decrease Decrease Increase Decrease
Decrease Increase No change Decrease Increase
Decrease Increase Increase Decrease Increase
Handgrip Squatting
decrease
Amyl
Nitrite
Increase Increase
Leg
Raising
Aortic Regurgitation
Etiology. Systemic hypertension and ischemic heart disease are the most common causes of
aortic regurgitation.
• It may occur after infectious endocarditis.
• Conditions that may affect the ascending aorta and cause aortic regurgitation:
– Syphilis
– Ankylosing spondylitis
– Marfan syndrome
– Rheumatic fever
– Aortic dissection
– Aortic trauma
Pathophysiology
Aortic regurgitation results in a volume overload of the left ventricle.
• The ventricle compensates by increasing its end-diastolic volume according to the
Frank-Starling mechanism.
•
The left ventricular dilation is thought to overstretch the myofibrils, leading to less
actin–myosin interaction and decreased contractility.
• In acute severe aortic regurgitation, the left ventricle has not had the opportunity to
dilate, its compliance is relatively high, and the aortic regurgitation therefore leads to
very high left ventricular end-diastolic pressure.
If mitral regurgitation ensues, the elevated left ventricular diastolic pressure is reflected back
to the pulmonary vasculature, and acute pulmonary edema may occur.
Acute aortic regurgitation results in a lower cardiac output, narrower aortic pulse pressure,
and a smaller left ventricle than does chronic aortic regurgitation.
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USMLE Step 2 CK
l Internal Medicine
Aortic diastolic pressure decreases in chronic aortic regurgitation because of both the regurgitation of blood into the left ventricle and a compensatory decrease in systemic vascular
resistance to maintain forward cardiac flow to the periphery. The increased pulse pressure in
chronic aortic regurgitation is due to the large stroke volume, causing increased systolic and
decreased diastolic pressure.
Clinical Manifestations
• Dyspnea is the most common complaint.
• Diastolic decrescendo murmur is the most typical.
• Systolic flow murmur
• Duroziez sign: Systolic and/or diastolic thrill or murmur heard over the femoral arteries
• S3 in early left ventricular decompensation
• Austin-Flint murmur
• Remember: Aortic regurgitation can cause 3 different murmurs.
Diagnosis
• EKG: LV hypertrophy often with volume overload pattern (narrow deep Q waves in
left precordial leads)
• Chest x-ray: LV and aortic dilation
• Echocardiography: Dilated LV and aorta; left ventricular volume overload; fluttering of
anterior mitral valve leaflet
Treatment. Endocarditis prophylaxis is no longer recommended.
• Salt restriction, diuretics, after load reduction (e.g., ACE inhibitors)
• Aortic valve replacement when symptoms worsen or ejection fraction decreases.
• Vasodilators such as an ACE, ARB, or nifedipine are the standard of care.
• Perform surgery when the ejection fraction is <55% or left ventricular systolic diameter is >55 mm.
Cardiomyopathy
Definition. A disease involving the heart muscle itself.
Classification. Cardiomyopathies can be classified according to morphologic and hemody-
namic characteristics.
152
Table 5-11. Morphologic and Hemodynamic Characteristics of Cardiomyopathies
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Dilated Hypertrophic Restrictive
Chapter 5
l Cardiology
Biventricular
dilatation
Cardiac output
Stroke volume
Ventricular
filling pressure
Chamber size
Ejection
fraction
Diastolic
compliance
Other findings May have associated
↓
↓
↑
↑
↓ ↑
Normal
functional mitral
or tricuspid
regurgitation.
Marked hypertrophy
of left ventricle and
occasionally of right
ventricle; can have
disproportionate
hypertrophy of
septum
Normal or ↓ Normal to ↓
Normal or ↑ Normal or ↓
Normal or ↑
Normal or ↓ Normal or ↑
↓ ↓
Obstruction may
develop between
interventricular
septum and septal
leaflet of mitral valve.
Reduced ventricular
compliance; usually
caused by infiltration
of myocardium
(e.g., by amyloid,
hemosiderin, or
glycogen deposits)
↑
Normal to ↓
Characteristic
ventricular
pressure tracing
that resembles
those recorded
in constrictive
pericarditis, with
early diastolic
dip-and-plateau
configuration
Characterized by diminished myocardial contractility, usually involving both ventricles; most
common cause for heart transplants.
Etiologies of Dilated (Congestive) Cardiomyopathy
• Idiopathic: most common
• Alcoholic
• Peripartum
• Postmyocarditis due to infectious agents (viral, parasitic, mycobacterial, Rickettsiae)
• Toxins (cobalt, lead, arsenic)
• Doxorubicin hydrochloride, cyclophosphamide, vincristine
• Metabolic: chronic hypophosphatemia, hypokalemia, hypocalcemia, uremia
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USMLE Step 2 CK
l Internal Medicine
Clinical Manifestations. Symptoms and signs of left and right ventricular failure. Typical
symptoms of systolic dysfunction.
Diagnosis
• X-ray: cardiomegaly with pulmonary congestion
• EKG: sinus tachycardia, arrhythmias, conduction disturbances
• Echo (key diagnostic study): dilated left ventricle, generalized decreased wall motion,
mitral valve regurgitation; transesophageal echo is more sensitive and specific than
transthoracic
• Catheterization: dilated hypocontractile ventricle, mitral regurgitation
Treatment. Patients are treated as those with systolic heart failure. ACE, beta blockers, and
spironolactone lower mortality. Diuretics and digoxin decrease symptoms. Implantable defibrillator may decrease risk of sudden death when the ejection fraction is <35%.
Hypertrophic Obstructive Cardiomyopathy
Etiology. Although hypertrophic obstructive cardiomyopathy (HOCM) can apparently develop
sporadically, it is hereditary in >60% of cases and is transmitted as an autosomal dominant trait.
• An abnormality on chromosome 14 has been identified in the familial form of the
disease.
• The distinctive hallmark of the disease is unexplained myocardial hypertrophy, usually
with thickening of the interventricular septum.
Pathophysiology. As a result of the hypertrophy, left ventricular compliance is reduced, but
systolic performance is not depressed. Diastolic dysfunction is characteristic, resulting in
decreased compliance and/or inability for the heart to relax.
• The heart is hypercontractile, and systole occurs with striking rapidity.
• Ejection fractions are often 80–90% (normal is 60%, ±5%), and the left ventricle may
be virtually obliterated in systole.
• The ability to provoke obstruction or increase/decrease already existing obstruction is
influenced by several factors.
154
Table 5-12. Factors That Modify Obstruction in Hypertrophic Obstructive Cardiomyopathy
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Increase Obstruction Decrease Obstruction
Chapter 5
l Cardiology
Mechanism Physiologic or
Pharmacologic Factors
Increase in
contractility
Reduction in
preload
Reduction in
afterload
Tachycardia
Digitalis glycosides
b-adrenergic stimulation
(e.g., epinephrine,
exercise)
Premature beats
Valsalva maneuver
Decrease in intravascular
volume
Standing
Nitroglycerin
Vasodilator drugs
Tachycardia
Hypovolemia (diuretics)
Nitroglycerin and related
drugs
Vasodilator drugs
Mechanism Physiologic or
Pharmacologic Factors
Decrease in
contractility
Increase in
preload
Increase in
afterload
b-adrenergic blockade
Heavy sedation and general
anesthesia
Calcium channel blockers,
disopyramide, and
other drugs that depress
myocardial function
Intravascular volume
expansion
Squatting
Bradycardia
b-adrenergic blockade
Intravascular volume
expansion
Squatting
a -adrenergic stimulation
(e.g., phenylephrine)
Handgrip
Clinical Manifestations
• Dyspnea, angina, presyncope, syncope with exertion, and palpitations
• Large jugular A wave, bifid carotid pulse, palpable S4 gallop, systolic murmur and
thrill, mitral regurgitation murmur
• Sudden death can sometimes be the first manifestation.
Diagnosis
• EKG: left ventricular hypertrophy, pseudo Q waves (often seen V1–V3), ventricular
arrhythmias
• Echocardiogram is the mainstay of diagnosis. It typically shows hypertrophy, systolic
anterior motion of mitral valve, and midsystolic closure of aortic valve
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USMLE Step 2 CK
l Internal Medicine
Clinical Pearl
With HOCM, avoid the
following:
• Digitalis
• Diuretics
• Vasodilators
• Exercise
Treatment
• Beta-blockers
• Calcium channel blockers that reduce heart rate: diltiazem, verapamil
• Disopyramide, occasionally
• Use implantable defibrillator if there is syncope
• Surgery in severe cases—septoplasty
Restrictive Cardiomyopathy
Restrictive cardiomyopathy is the least common of the causes of cardiomyopathy. It is myocardial disorder characterized by rigid noncompliant ventricular walls.
Etiologies
• Infiltrative: sarcoidosis/amyloidosis; hemochromatosis; neoplasia
• Scleroderma
• Radiation
Pathophysiology. The myocardium is rigid and noncompliant, impeding ventricular filling
and raising cardiac filling pressures from abnormal diastolic function. Systolic performance is
often reduced, but the overriding problem is impaired diastolic filling, which produces a clinical and hemodynamic picture that mimics constrictive pericarditis.
Clinical Manifestations
• Dyspnea, exercise, intolerance, weakness
• Elevated jugular venous pressure, edema, hepatomegaly, ascites, S4 and S3 gallop,
Kussmaul sign
Diagnosis
• X-ray: mild cardiomegaly, pulmonary congestion
• EKG: low voltage, conduction disturbances, Q waves
• Echo: characteristic myocardial texture in amyloidosis with thickening of all cardiac
structures
• Catheterization: square root sign; elevated left- and right-sided filling pressures
Treatment. There is no good therapy; ultimately results in death from CHF or arrhythmias;
consider heart transplantation.
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Acute Pericarditis
Figure 5-11. Acute Pericarditis with Diffuse ST Segment Elevation
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Definition. Inflammation of the pericardial lining around the heart.
Chapter 5
l Cardiology
I
II
III V3 V6
II
Etiology
• Idiopathic
• Infections (viral)
• Vasculitis—connective tissue disease group
• Disorders of metabolism
• Neoplasms
• Trauma
• Inflammation—uremia
aVR V1 V4
aVL V2 V5
aVF
Clinical Manifestations. Chest pain, often localized substernally or to the left of the sternum, is
usually worsened by lying down, coughing, and deep inspiration (which helps in the differential
diagnosis with MI) and is relieved by sitting up and leaning forward.
Pericardial friction rub (diagnostic of pericarditis) is a scratchy, high-pitched sound that has
1 to 3 components corresponding to atrial systole, ventricular systole, and early diastolic ventricular filling. The ventricular systole component is present more consistently. The rub is
often transient and is best heard with the diaphragm of the stethoscope as the patient sits forward at forced-end expiration.
Diagnosis. EKG may be diagnostic and reveals a diffuse ST-segment elevation with upright
T waves at the onset of chest pain. PR segment depression is very specific.
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USMLE Step 2 CK
l Internal Medicine
Differential Diagnosis. The diffuseness of the ST-segment elevation, absence of reciprocal
leads, and absence of the development of Q waves distinguish the characteristic pattern of acute
pericarditis from the pattern seen in acute MI.
Treatment of the patient with acute pericarditis involves treating its etiology. In idiopathic
pericarditis, treatment with anti-inflammatory medications (NSAIDs, aspirin, corticosteroids)
is appropriate. Adding colchicine to an NSAID decreases recurrence.
Pericardial Effusion
Etiology. Fluid may accumulate in the pericardial cavity in virtually all forms of pericardial disease. The fluid may be a transudate, as are the serous cavity effusions that develop in
patients with CHF, overhydration, or hypoproteinemia. More often, however, the pericardial
effusion is an exudate, reflecting the presence of pericardial injury.
• Serosanguineous pericardial fluid is a classic sign in tuberculosis and neoplastic diseases.
• Frank blood in the pericardial space may occur in cases of aortic aneurysm or aortic
dissection.
• Hemopericardium may also be produced by closed or penetrating trauma, rupture of
the heart in acute MI, and bleeding caused by coagulation defects.
• When fluid accumulates slowly, the pericardium expands to accommodate it. When
fluid accumulates rapidly, however, it compresses the heart and inhibits cardiac filling
(cardiac tamponade).
Diagnosis. Echocardiography is the most effective laboratory technique available. The presence of pericardial fluid is recorded as a relatively echo-free space between the posterior
pericardium and the posterior left ventricular epicardium in patients with small effusions. In
patients with large effusions, the heart may swing freely within the pericardial sac, and this
motion may be associated with electrical alternans.
Chest x-ray may show a “water-bottle” configuration of the cardiac silhouette.
Treatment
• Fluid aspiration
• Management of acute pericarditis etiology
Definition. A life-threatening condition in which a pericardial effusion has developed so rapidly or has become so large that it compresses the heart.
Etiology
• Neoplasia
• Idiopathic (usually viral) pericarditis
• Nonviral infection
– Tuberculous
– Suppurative
• Intrapericardial hemorrhage with or without pericarditis
158
• Wounds, including surgery of
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– Chest
– Heart
– Pericardium
• Postpericardiotomy syndrome
• Uremia
• Mediastinal and juxtamediastinal radiation therapy
• Vasculitis–connective tissue disease group
Clinical Manifestations. Most patients with cardiac tamponade complain of dyspnea, fatigue,
and orthopnea.
• Pulsus paradoxus, characterized by a decrease in systolic blood pressure >10 mm Hg
with normal inspiration, frequently is present. The paradoxical pulse often can be
noted by marked weakening or disappearance of a peripheral pulse during inspiration.
Paradoxical pulse is not diagnostic of cardial tamponade and can occur in chronic
lung disease, acute asthma, severe CHF, and in some cases of hypovolemic shock.
• Neck vein distension with clear lung
• Shock (hypotension)
• Decreased heart sounds
• Beck’s triad is associated with acute tamponade; it includes low blood pressure, distended neck veins, and decreased heart sounds
Chapter 5
l Cardiology
Diagnosis. Clinical manifestations followed by echocardiography and cardiac catheterization,
which confirms that left and right atrial pressures are equal.
Treatment
• Pericardiocentesis
• Subxiphoid surgical drainage
Constrictive Pericarditis
Definition. The diffuse thickening of the pericardium in reaction to prior inflammation,
which results in reduced distensibility of the cardiac chambers.
• Cardiac output is limited and filling pressures are increased to match the external constrictive force placed on the heart by the pericardium.
•
The fundamental hemodynamic abnormality is abnormal diastolic filling.
Etiologies
• Idiopathic, unknown
• Following open-heart surgery
• Following thoracic radiation
• Postviral infection
Clinical Manifestations. Most patients complain of dyspnea on exertion due to limited cardiac
output. Orthopnea occurs in about 50% of patients. Symptoms and signs related to systemic
venous hypertension are often reported and include ascites, edema, jaundice, hepatic tenderness,
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