At the end of each explained answer, there is a number combination in parentheses. The first number identifies the reference source; the second number or set of numbers indicates the page or pages on which the relevant information can be found.
1. (D) The coronary or atrioventricular groove separates the atria from the ventricles. Within this groove lies the main trunk of the coronary arteries and the coronary sinus. (31:13)
2. (F) (31:378)
3. (D) (31:378)
4. (B) (31:378)
5. (E) (31:378)
6. (H) (31:378)
7. (C) (31:378)
8. (I) (31:378)
9. (A) (31:378)
10. (G) (31:378)
11. (D) Indications for stress echocardiography do not include unstable angina. In fact, this is a contraindication for stress echocardiography. (31:138)
12. (C) Transesophageal echocardiography (TEE) is performed by a physician with specialized training in TEE performance and interpretation. TEE is routinely used to evaluate cardiac structure and function, although it is considered more invasive than a transthoracic or surface echocardiogram. (31:209)
13.(E) The purpose of the pericardium is to (1) reduce friction with the cardiac movement, (2) allow the heart to move freely with each beat, facilitating ejection and volume changes, (3) contain the heart within the mediastinum, especially during trauma, and (4) serve as a barrier to infection, whereas the grooves or sulci separate the heart chambers and contain the vessels. (31:12, 13)
14. (D) Left ventricle. In the adult, the left ventricle is larger and has an outer wall that is 8–12 mm thick. (31:16)
15. (D) There are four pulmonary veins, two from each lung. They carry oxygenated blood from the lungs to the left atrium of the heart. (31:14)
16. (C) The right atrium has two parts: an anterior portion and a posterior portion. These two portions are separated by a ridge of muscle called the crista terminalis. (Study Guide: 106)
17. (B) The mitral valve is an atrioventricular valve that is located between the left atrium and the left ventricle. (31:14, 15)
18. (B) The normal pressure in the right ventricle is approximately 15–30 mm Hg. (Study Guide: 106)
19. (D) Mitral valve stenosis results primarily from rheumatic disease. The valves may not become involved for many decades following rheumatic fever. Other rare causes include congenital mitral stenosis, calcification of the mitral annulus that involves the mitral leaflets, thrombus, vegetations, atrial myxomas, and parachute mitral valve deformity. (31:241)
20. (C) Endocarditis. Endocarditis is caused by bacterial, yeast, or fungal infections that seed and grow on the valves of the heart, papillary muscles, and in some cases, the endocardial surface of the ventricles. Vegetations, commonly associated, form as a result of complex interactions between the immune system, the coagulation system, hemodynamic forces, and the invading microorganisms. (31:477)
21. (D) Bjork–Shiley is a tilting disc valve that is a mechanical prosthetic valve. The xenograft, heterograft, homograft, and allograft are all bioprosthetic heart valves. (31:310, 311)
22. (D) The normal intrapericardial space contains 15–50 mL of fluid. In cases of pericardial effusion as the fluid is added rapidly, the intrapericardial pressure increases dramatically. Initially, pericardial effusion is recognized in the posterior basal region, and as it increases, it occurs medially and laterally and involves the apex. (31:489)
23. (C) The term cardiomyopathy is used to describe a variety of cardiac diseases that affect the myocardium. Cardiomyopathies affect an otherwise structurally normal heart and are classified into three categories: hypertrophic, dilated, and restrictive. (31:586)
24. (A) Myxoma is the most common benign tumor of the heart. Almost 75% of all primary tumors are benign, with myxomas accounting for almost half of this group. They can occur in all age groups. (31:463)
25. (D) Angiosarcomas are the most common malignant cardiac tumors of the heart. They usually occur in adults and are more frequent in men. They are soft tissue tumors of the blood vessels and lymphatic endothelium. (31:467)
26. (D) A dissecting aneurysm results from intimal tears of the aortic wall. The driving force of the blood destroys the media and strips the intimal layer from the adventitial layer. They are classified as a Type I, II, or III, according to the area and extent of the intimal tear. (31:606, 607)
27. (D) Abnormalities of the left ventricular outflow tact are the most common congenital heart disease in the adult population, with obstruction occurring at the subvalvular, supravalvular, or valvular level. (Study Guide)
28. (D) In adults tetralogy of Fallot is the primary congenital disease producing cyanosis. It comprises four defects: aorta overriding intraventricular septum IVS, ventricular septal defect (VSD), infundibular stenosis, and right ventricular hypertrophy. (31:549)
29. (B) Pericarditis is not a characteristic of cardiomyopathy. Cardiomyopathy is a term describing a variety of cardiac diseases affecting the myocardium. They are classified into three categories according to the characteristics. The categories are hypertrophic, dilated, and restrictive. (31:586–588)
30. (A) (31:28)
31. (F) (31:28)
32. (G) (31:28)
33. (B) (31:28)
34. (D) (31:28)
35. (E) (31:28)
36. (C) (31:28)
37. (C) Right atrium. In stenotic disease of the tricuspid valve, the effects on atria, ventricles, and vessels cause dilatation of the right atrium. Tricuspid stenosis is most often caused by rheumatic heart disease but can also be caused by such other conditions as: systemic lupus erythematosus, carcinoid heart disease, Loffler’s endocarditis, metastatic melanoma, and congenital heart disease. (31:295, 296)
38. (D) In tricuspid valve disease, the primary cause of regurgitation is secondary to pulmonary hypertension. In rare cases, regurgitation can be caused by rheumatic heart disease. (31:297)
39. (A) Ebstein’s anomaly of the tricuspid valve is a condition where the tricuspid valve leaflets are displaced toward the apex of the right ventricle. (31:571)
40. (B) Dyspnea on exertion. Clinical symptoms of aortic valve stenosis include chest pain, shortness of breath, and syncope. Most patients do not develop these classic symptoms until the degree of aortic stenosis is moderate to severe. (31:277)
41. (D) The mitral valve has two major leaflets and is the only cardiac valve with this characteristic; therefore, it is occasionally called the bicuspid valve. (31:15)
42. (D) The classic clinical finding in mitral valve prolapse is a systolic click, which corresponds with the posterior displacement of the mitral valve leaflet into the left atrium, and a late systolic murmur, which corresponds with the resulting mitral regurgitation that often occurs because of the prolapsing leaflets. (31:263)
43. (A) The most common cause of flail leaflet is rupture of the chordae tendineae, which often occurs secondary to myocardial infarction. Rupture of the papillary muscle is a less common etiology. The chordae tendineae support the leaflets and prevent them from prolapsing during systole. (31:19)
44. (D) Transesophageal echocardiography provides complete evaluation of all regions of the heart, including the great vessels. It provides higher resolution because of the transesophageal window, allowing the use of higher-frequency transducers. (31:92)
45. (C) The coronary sinus is guarded by the thebesian valve. This valve is often continuous with the eustachian valve. (31:18)
46. (A) The average length of an adult heart is 12 cm, width 8–9 cm in the broadest diameter, and 6 cm at its narrowest portion. The weight is roughly 280–340 g in men and 230–280 g in women. Cardiac weight is approximately 0.45% of total body weight in men and 0.40% of total body weight in women. (31:12, 13)
47. (D) The atrioventricular node and its atrial branches are located in a triangular zone lying between the attachment of the septal leaflet of the tricuspid valve, the anteromedial orifice of the coronary sinus, and the tendon of Todaro. It is referred to as the triangle of Koch. (31:17)
48. (B) Superior vena cava. The blood circulates through the body and returns to the heart to be transported to the lungs for reoxygenation. The inferior vena cava drains the trunk and lower extremities and the superior vena cava drains the head and parts of the upper extremities. (31:17)
49. (C) Subcostal. Standard parasternal and suprasternal views do not demonstrate all four cardiac chambers. Only the apical and subcostal windows allow visualization of all cardiac chambers. (1:80)
50. (A) Long axis, short axis, and four chamber. The American Society of Echocardiography has standardized two-dimensional views of the heart into three basic orthogonal planes for which all views can basically be categorized. (2:212)
51. (A) Atrial septal defects and ventricular septal defect. If the ultrasound beam is not oriented perpendicular to the interatrial and interventricular septum, there may be false dropout of echoes. The subcostal approach allows the ultrasound beam to be perpendicular to the cardiac chambers, thereby allowing a better demonstration of atrial or ventricular septal defects. In addition, any gap noted in the interatrial or interventricular septum when the subcostal four-chamber view is used should be considered real. (1:92)
52. (B) Time-gain compensation. The time-gain compensation control allows the echocardiographer to selectively increase or decrease the gain at different depths of tissue. The objective is to achieve a uniform echocardiographic image without artifactually adding or eliminating information. (3:52)
53. (A) The right ventricular pressure drops below the right atrial pressure. The atrioventricular valves open when ventricular pressure drops below atrial pressure. (3:38)
54. (B) The coronary ligament. This ligament defines the bare area of the liver and is the only choice that does not represent a remnant of fetal circulation. (4:30)
55. (A) Pulmonary artery. The right side of the heart pumps deoxygenated blood through the pulmonary artery to the lungs for reoxygenation. (The pulmonary artery is the only artery in the body that carries deoxygenated blood.) (3:9)
56. (C) Left atrium. Four pulmonary veins transport oxygenated blood from the lungs to the left atrium. (The pulmonary veins are the only veins in the body that carry oxygenated blood.) (3:9)
57. (D) The left ventricle constitutes most of the ventral surface of the heart. The right ventricle, though less muscular than the left ventricle, dominates the ventral surface of the heart. (3:25)
58. (A) Aortic valve opening and closing points. Left ventricular ejection time—the time it takes for blood to be ejected from the left ventricle—can be obtained from an M-mode tracing of the aortic valve by measuring the time interval between opening and closing of the valve. (3:156)
59. (D) Subcostal. Lung expansion in patients with chronic obstructive pulmonary disease often obliterates the apical and parasternal position. This lung expansion also tends to shift the heart inferiorly, making the subcostal view the best approach for scanning the heart. (5:79)
60. (B) Apical and right sternal border. The most common windows used to record systolic blood flow across the aortic valve are the apical, right parasternal, and suprasternal. (6:128)
61. (A) At end-systole. M-mode measurements of the left atrium, left ventricle, and right ventricle are done at a point when the chambers are at their largest. The left atrium is largest at end-systole. (3:82)
62. (C) Stenosis. Doming is a main two-dimensional feature of any stenotic valve. The valve domes when it opens because the commissures are fused, causing the body of the valve to separate more widely than the tips. (1:251)
63. (C) Perpendicular, parallel. Because of the differences in transducer orientation for optimum two-dimensional and Doppler studies, one rarely obtains excellent quality images and waveforms simultaneously and may have to relinquish quality in one to obtain excellent-quality images in the others. (1:104)
64. (D) Pulmonary hypertension. The constant pressure overload of pulmonary hypertension causes right ventricular hypertrophy until the ventricle fails, at which point the right ventricle wall dilates. (3:217)
65. (C) Chordae tendineae. Left ventricular dimensions have been standardized to be obtained at the level of the chordae tendineae. (7:1072)
66. (C) Left ventricular volume overload. Right ventricular volume overload may cause paradoxical interventricular septal motion (anterior motion of the interventricular septum at the onset of systole). (1:164)
67. (A) Toward the right ventricular free wall. Right ventricular volume overload causes paradoxical septal motion, whereby the septum moves toward the right side of the heart in systole rather than toward the left side of the heart. (1:164)
68. (A) Organic in origin. A thrill is a murmur that produces a vibratory sensation when palpated. It is almost always organic in origin. (8:51)
69. (A) Mitral valve prolapse or systolic anterior motion of the mitral valve. The Valsalva maneuver and the inhalation of amyl nitrite decrease left ventricular volume and reduce the diameter of the left ventricular outflow tract, thereby stimulating mitral valve prolapse or systolic anterior motion of the mitral valve. (3:222)
70. (A) Cyanotic heart disease. Clubbing occurs when there is widening and cyanosis of the distal ends of the fingers and toes. (9:18)
71. (B) Providing enhanced temporal resolution. M-mode is still used in many laboratories to take measurements and to evaluate events that occur too rapidly for the eye to perceive such as diastolic fluttering of the anterior mitral leaflet. This is the case because M-mode provides far better temporal (time) resolution than does two-dimensional echocardiography and allows for better analysis of intracardiac events. (3:78)
72. (C) To a higher intercostal space. If the transducer is placed too low relative to the position of the heart, the sector plane passes obliquely through the left ventricle, producing an ovoid image. (3:110)
73. (C) Decreased left ventricular compliance. This situation, referred to as reversed E-to-A ratio, indicates decreased left ventricular diastolic compliance. Conditions that cause this include left systemic hypertension, hypertrophic cardiomyopathy, and coronary artery disease. (3:240)
74. (C) A left ventricular thrombus. Left ventricular function is not impaired in mitral stenosis. Because thrombi tend to form in areas of poor blood flow, the likelihood of finding a left ventricular thrombus is low. (1:489)
75. (D) A peak gradient occurring in late diastole. The peak gradient in mitral stenosis usually occurs in early diastole. (10:132)
76. (C) Mitral insufficiency. Ruptured chordae tendineae always result in mitral regurgitation, the onset of which is often abrupt and acute. (3:189)
77. (D) Hypertrophic obstructive cardiomyopathy. This causes anterior motion of the mitral valve. It is not a source of confusion for mitral valve prolapse, in which the mitral valve moves posteriorly in systole. (11:211)
78. (A) A dilated left atrium. This is a secondary sign of mitral regurgitation. The left ventricle usually dilates as well and becomes hyperkinetic in response to the volume overload. (1:266)
79. (A) Width and length of the systolic jet by color Doppler. Color Doppler provides a spatial display of regurgitant flow. Quantification of the severity of mitral regurgitation is based roughly on the size and configuration of the regurgitant jet. (12:87)
80. (D) Pulmonic stenosis. The pulmonic valve is the valve that is least likely to be deformed by rheumatic fever. When pulmonic stenosis is noted on an echocardiogram, it is usually a congenital abnormality rather than a sequela of rheumatic fever. (9:1711)
81. (A) A dilated left atrium and left ventricular hypertrophy. Mitral stenosis causes the left atrium to dilate, and aortic stenosis leads to left ventricular hypertrophy. (3:186, 206)
82. (B) Concurrent atrial fibrillation. Mitral stenosis often leads to atrial fibrillation. The A wave of the mitral valve corresponds to the P wave on the electrocardiogram. Because the P wave is absent in atrial fibrillation, the A wave will be absent as well. (11:333)
83. (B) Hypertrophic cardiomyopathy. Under normal circumstances, the mitral E point, which represents rapid ventricular filling, is higher than the mitral A point, which corresponds to atrial contraction. This relationship between the two points is altered when there is decreased left ventricular compliance (as is the case with hypertrophic cardiomyopathy). (6:155)
84. (B) Aortic regurgitation. Aortic regurgitation causes a left ventricular volume overload pattern on the echocardiogram (a dilated and hypercontractile left ventricle). Mitral regurgitation usually causes dilatation of both the left atrium and the left ventricle. (5:231)
85. (C) A decreased E–F slope, a thickened mitral valve, and a mitral distal velocity >1.5 m/s. Both thickening of the mitral valve and a reduced E–F slope must be noted to be sure the pathology is mitral stenosis. Diastolic doming of the mitral valve also is a specific sign of mitral stenosis. (1:251)
86. (B) An increased E–F slope on M-mode. One M-mode criterion for mitral stenosis is a decreased E–F slope. (1:249)
87. (C) Tips of the mitral leaflets. The mitral valve is funnel shaped, with the true orifice at the narrow end. Measurement of the size of the orifice should therefore be done at the tips of the leaflets at the point where the chordae tendineae merge with the body of the valve. (3:161)
88. (C) A dilated left ventricle. Unless there is concomitant mitral regurgitation, the size of the left ventricle will be normal or smaller than normal. (13:64)
89. (C) An increase in pressure half-time. A successful mitral valve commissurotomy should lead to a decrease in the pressure half-time. The other findings will usually remain, although the left atrium may decrease slightly in size. (13:65)
90. (B) Concomitant mitral regurgitation. Pure mitral stenosis leads to a dilated left atrium and a normal or smaller-than-normal left ventricle. Aortic stenosis and hypertrophic cardiomyopathy cause the left ventricular walls to appear thickened. Only concomitant mitral regurgitation will cause left ventricular dilatation as well. (1:139)
91. (A) Severe acute aortic regurgitation. Severe acute aortic insufficiency can cause an elevated left ventricular diastolic pressure, which, in turn, causes the mitral valve to close early. (1:295)
92. (D) A ventricular septal defect. Such conditions as systemic hypertension that stress the area of the mitral annulus can lead to premature calcification of the mitral annulus. (9:1035)
93. (B) 1 cm. Studies by Hatle and coworkers found that a mitral valve with an area of 1 cm exhibits a Doppler pressure half-time of 220 m/s. (14:1096)
94. (B) Diastolic fluttering of the anterior mitral leaflet. This is a finding of aortic insufficiency. (3:210)
95. (D) Systemic hypertension. This produces pressure overload of the left ventricle that, in turn, leads to left ventricular hypertrophy. Choices B and C cause a left ventricular volume overload pattern on the echocardiogram (dilated and hyperkinetic left ventricle). (15:104)
96. (C) Aortic stenosis. A systolic ejection murmur can be heard with this disorder. (3:204)
97. (C) It is often seen in conjunction with mitral stenosis. A bicuspid aortic valve is a congenital abnormality in which one of the aortic commissures is fused, leading to the formation of two aortic cusps instead of the usual three. Bicuspid valves tend to become stenotic in adulthood. Although they are sometimes seen in conjunction with Coarctation of the Aorta, a bicuspid valve and mitral stenosis have no direct association. (3:202)
98. (B) Aortic valve area, poor left ventricular function. When aortic stenosis is found in conjunction with a poorly moving left ventricle, standard estimations of the degree of aortic stenosis will be inaccurate. The continuity equation compensates for ventricular hypocontractility, allowing for a more accurate estimate of the aortic valve area. (3:207; 16:105)
99. (B) The mean pressure gradient. Aortic insufficiency may cause a high initial instantaneous gradient. When there is combined aortic stenosis and insufficiency, the mean pressure gradient is more specific for estimating the severity of aortic stenosis. (6:137)
100. (A) The apical long-axis view. All Doppler procedures are best performed with the ultrasound beam directed parallel to the flow of blood. Of the choices presented, the apical long-axis view provides the optimum angle to image acquisition. (1:104)
101. (B) Left ventricular hypertrophy. Aortic stenosis causes pressure overload of the left ventricle. This overload leads to left ventricular hypertrophy. (11:203)
102. (A) Aortic insufficiency. The anterior mitral leaflet flutters rapidly when hit by an aortic insufficiency jet. These oscillations are best detected by M-mode. Atrial fibrillation causes coarse diastolic fluttering of the anterior mitral leaflet. (1:294)
103. (D) Consistent with moderate aortic regurgitation. The grading of aortic insufficiency with Doppler echocardiography is similar to the grading method used in cardiac catheterization laboratories. An aortic insufficiency jet that extends from the aortic valve to the tips of the anterior mitral leaflet is consistent with moderate aortic regurgitation. (17:339)
104. (B) Fine diastolic fluttering and possible flattening of the anterior mitral leaflet. An Austin-Flint murmur represents functional mitral stenosis caused by inhibition of anterior leaflet motion resulting from compression by a strong aortic insufficiency jet. This would appear on M-mode as fine diastolic fluttering of the anterior mitral leaflet with inhibition of opening. (9:77)
105. (D) Right sternal border view. When obtainable, the right sternal border approach is usually best for acquiring maximum aortic valve velocities. The patient is turned onto his or her right side, and the Doppler probe is directed into the aortic root. (18:89)
106. (D) Transesophageal echocardiography. Because of the high-resolution images it provides of the thoracic aorta, transesophageal echocardiography has been highly successful in evaluating patients with suspected aortic dissection. (19:216)
107. (D) A thickened anterior right ventricle wall. Thickening of the right ventricular walls is usually caused by right ventricular pressure overload. Tricuspid insufficiency causes right ventricular volume overload. (1:162)
108. (D) Pulmonary hypertension. The right ventricular systolic pressure in this ventricle is approximately 74 mm Hg (using the formula 4 V2 + 10). Because right ventricular pressures are basically equal to pulmonary artery pressures, the pulmonary artery pressure in this instance is roughly 74 mm Hg, thus indicating the presence of pulmonary hypertension. (3:161)
109. (D) It is usually seen as part of the aging process. Tricuspid stenosis is a rare condition that usually occurs as a sequela to rheumatic fever. Its echocardiographic findings are similar to those of mitral stenosis. (3:198)
110. (C) Contrast in the inferior vena cava during ventricular systole. With severe tricuspid regurgitation, the regurgitant volume extends all the way back into the right atrium and sometimes into the inferior vena cava as well. By injecting contrast, this regurgitant volume can be “seen” with M-mode or two-dimensional echocardiography. (1:305)
111. (B) Tricuspid valve. The echocardiographer should pay special attention to this valve because carcinoid heart disease presents as thickening and rigidity of the tricuspid valve leaflets. Severe tricuspid regurgitation is usually detected with Doppler. (1:305)
112. (B) Right ventricular systolic pressure. By using the modified Bernoulli equation and an estimate of jugular venous pressure, systolic pressure in the right ventricle can be determined. (3:112)
113. (C) Infundibular pulmonic stenosis. This is caused by hypertrophied muscle bands in the right ventricular outflow tract. Echocardiographically, it can be distinguished from valvular pulmonic stenosis by noting a step-up in Doppler velocities proximal to the pulmonic valve. In addition, the muscular ridge produces turbulence of blood, which hits the pulmonic valve and causes it to flutter. (1:393)
114. (D) Left parasternal. Pulmonary artery flow velocities are usually obtained from the left parasternal short-axis view at the level of the aortic root. (10:80)
115. (A) Cranial and lateral. This relationship is best appreciated from the short-axis view of the base of the heart. (3:27)
116. (C) Midsystolic notching noted on M-mode. Midsystolic notching is a sign of pulmonary hypertension. (3:388)
117. (B) Two-dimensional echocardiography. The spatial orientation of two-dimensional echocardiography provides for a better assessment of the size, location, and motion of valvular vegetations. (3:277)
118. (B) Mitral valve vegetation. Intravenous drug abusers have an increased incidence of endocarditis because of microorganisms that enter the bloodstream via unsterile needles. Vegetations usually form on the valves of the right side of the heart, but they may settle on left-sided valves as well. One complication of valvular vegetation is an embolic event. (3:276)
119. (B) Presence of paravalvular regurgitation. The spatial orientation of color Doppler allows for a quick assessment of blood flow in the region surrounding the prosthetic valve. (12:141)
120. (A) May exhibit high Doppler velocities. The normal Doppler velocities across any prosthetic valve will be slightly higher than those of a native valve. A Starr-Edwards, or ball-in-cage, valve tends to exhibit the highest velocities. (3:349)
121. (A) An example of a mechanical heart valve. The Bjork–Shiley is a tilting-disc mechanical heart valve. (3:314)
122. (C) Transesophageal echocardiography. This is a major application in the evaluation of prosthetic heart valves, particularly in the mitral position. (3:358)
123. (D) Hancock. This valve is an example of a heterograft (bioprosthetic) valve. (3:334)
124. (C) Abnormal rocking motion of the valve. Valve dehiscence refers to a condition in which the prosthetic valve loosens or separates from the sewing ring and causes an abnormal rocking motion and a paravalvular leak. (3:346)
125. (C) It often makes anticoagulation unnecessary. Mechanical valves require constant anticoagulation. Women during childbearing years would, therefore, be more likely to receive a bioprosthetic valve, which would not require anticoagulation. (20:1392)
126. (A) These patients are at a higher risk for endocarditis. Because bacteremias occur during dental or surgical procedures, prophylactic antibiotics are often administered to susceptible patients (such as mitral valve prolapse patients) in an attempt to prevent bacterial endocarditis. (20:1151)
127. (C) A “swinging heart” on the two-dimensional examination. Excessive motion of the heart can sometimes be noted with massive pericardial effusion. (1:558)
128. (A) It impairs diastolic filling. The rigid and fibrotic pericardial sac impairs diastolic filling of the cardiac chambers. (3:268)
129. (A) Pressure in the pericardial cavity rises to equal or exceed the diastolic pressure in the heart. Tamponade occurs when intrapericardial pressures rise and impair cardiac filling. Although cardiac tamponade is usually seen in association with a large pericardial effusion, a small effusion may cause tamponade if the rate of accumulation of pericardial fluid exceeds the ability of the pericardium to accommodate the increased volume. (15:213)
130. (D) In Dressler’s syndrome, a pericardial effusion develops as a result of renal disease. Dressler’s syndrome, also known as postmyocardial infarction syndrome, is the development of pericardial effusion 2–10 weeks after infarction. (9:1287)
131. (D) A pericardial effusion. Neoplasms from the thoracic region often lead to pericardial effusion. (20:1254)
132. (D) Mitral valve prolapse. The descending aorta, a calcified mitral annulus, and ascites can cause echo-free spaces that may be misleading on an echocardiogram. Although a large effusion in which the heart exhibits excessive motion may lead to false mitral valve prolapse, which will not lead to a false-positive diagnosis of pericardial effusion. (1:552)
133. (A) Pulmonic stenosis. Diastolic collapse of the right ventricular walls is a good indicator of tamponade. Pulmonic stenosis, or any other form of right ventricular pressure overload, leads to thickening of the right ventricular walls. A thickened wall is unlikely to collapse in diastole. (1:565)
134. (C) There is a large acoustic mismatch between lung tissue and pericardial tissue. A greater mismatch between two structures results in brighter reflected echoes from the interface between them. Because there is an extremely large acoustic mismatch between lung (air) and pericardium (tissue), the interface created by the two will cause a bright echo to appear on the echocardiogram. (1:2)
135. (C) Decreasing overall gain and increasing depth setting. Decreasing the gain allows for differentiation between the pericardium and epicardium, and increasing the depth setting helps define the borders of the effusion. (11:249)
136. (D) Descending aorta. Because the descending aorta lies posterior to the pericardial effusion and anterior to the pleural effusion, it often aids in differentiating between the two. (1:554)
137. (A) Constrictive pericarditis. The pericardium limits cardiac motion. When the pericardium is surgically removed (e.g., in constrictive pericarditis), the heart expands and exhibits excessive motion. (1:575)
138. (A) Excessive cardiac motion. Again, because the pericardium limits cardiac motion, the heart exhibits excessive motion when the pericardium is surgically removed. (1:575)
139. (C) Reduced compliance of the left ventricle. Systemic hypertension causes pressure overload of the left ventricle. As in all pressure-overload situations (e.g., aortic stenosis), the left ventricle hypertrophies and may become noncompliant, leading to diastolic dysfunction. (11:273)
140. (B) Left ventricular hypertrophy. This condition can be present in the absence of an obstruction. (1:522)
141. (D) Endomyocardial biopsy. Several echocardiographic signs are suggestive of amyloid heart disease, but a definitive diagnosis can be made only with an endomyocardial biopsy performed in the catheterization laboratory. (20:1215)
142. (B) Sarcoidosis. This is an infiltrative process that can lead to restrictive cardiomyopathy. (11:317)
143. (A) Increased systolic velocity in the left ventricular outflow tract. Velocities are low because of decreased cardiac output. (3:230)
144. (A) It is more likely to affect the right ventricle than the left ventricle. Cardiac contusion may be seen following a blunt trauma to the chest (such as a steering-wheel injury). Because the right ventricle is the most anterior structure of the heart, it is the one most susceptible to injury. (3:301)
145. (A) An apical aneurysm with a mural thrombus. Apical aneurysms sometimes develop following an anterior wall myocardial infarction. Because aneurysms are a likely site for thrombus, choice A is the most likely answer. (1:489)
146. (C) Two-dimensional demonstration of an ejection fraction lower than 50%. The ejection fraction is a measure of systolic left ventricular function. (20:51)
147. (C) Left anterior descending artery. This artery supplies the anterior wall of the left ventricle and the anterior portion of the interventricular septum. (3:237)
148. (D) They have a narrow neck. The best way to differentiate a true aneurysm from a pseudoaneurysm is to look at the width of its neck. Pseudoaneurysms tend to have a narrow neck because they result from a tear in the myocardium. (1:486)
149. (B) A reduced ejection fraction. An E point-to-septal separation of more than 10 mm correlates with a reduced ejection fraction. (11:205)
150. (B) Akinetic. Lack of systolic thickening and motion is referred to as akinesis. (11:287)
151. (D) Occlusion of the left anterior descending coronary artery. Blood to the inferior wall of the left ventricle is usually supplied by the right coronary artery. (1:467; 21:93)
152. (B) Severe mitral regurgitation. Doppler interrogation of a patient with ruptured papillary muscle will usually demonstrate this condition. (3:249)
153. (D) It is used in diagnosing ischemic heart disease. Stress echocardiography is used as an adjunct to standard stress testing in diagnosing patients with suspected coronary artery disease. Resting wall motion is compared to wall motion during and after stress. (3:250)
154. (C) They do not recur once they are surgically removed. Although characterized as a benign tumor, a myxoma may recur if some cells remain after excision of the tumor. (20:1285)
155. (B) Ventricular septal defects. The QP/QS ratio refers to the ratio of pulmonary-to-systemic blood flow. It can be calculated echocardiographically to determine the magnitude of left-to-right shunting of blood. (6:161)
156. (B) Continuous flow (systolic and diastolic) above baseline. Shunting of blood from the aorta to the pulmonary artery occurs in both systole and diastole. (18:220)
157. (B) Contrast injection echocardiography. Even a small atrial septal defect can be detected by noting the presence or absence of microbubbles. (1:406)
158. (B) Secundum. Atrial septal defects occur most commonly in the area of the foramen ovale, where they are termed ostium secundum defects. (3:381)
159. (C) Eisenmenger’s syndrome. In this syndrome, the pulmonary vascular resistance is equal to or greater than the systemic vascular resistance, leading to right-to-left shunting. (20:589)
160. (B) Infundibular pulmonic stenosis. In Ebstein’s anomaly, the tricuspid valve is large and partially adherent to the walls of the right ventricle so that the valve orifice is displaced apically. Therefore, most of the right ventricle functions as part of the right atrium. It is frequently associated with an atrial septal defect. Infundibular pulmonic stenosis is not part of the spectrum of this disorder. (3:406)
161. (D) Ostium primum atrial septal defect and an inlet ventricular septal defect. Endocardial cushion defects occur when the atrial and ventricular components of the cardiac septum fail to develop properly. (3:381)
162. (C) Descending thoracic aorta. Coarctation of the Aorta is a constrictive malformation of the aortic arch, usually located just distal to the origin of the left subclavian artery. The obstruction increases the velocity of blood flow beyond the point of constriction. (3:396)
163. (D) An atrial septal defect. The fourth component is right ventricular hypertrophy. (3:421)
164. (B) It is a congenital malformation in which a fibrous membrane divides the left atrium into an upper and lower chamber. Cor triatriatum is a rare abnormality in which an embryonic membrane in the left atrium fails to regress. It can be detected echocardiographically by noting a linear echo traversing the left atrium. Doppler echocardiography will detect high-velocity flow across a hole in the membrane. (3:402; 22:53)
165. (C) Paradoxical septal motion. Left bundle branch block often causes this motion. (1:231)
166. (C) A mechanical prosthetic valve. This high echogenicity of the mitral valve is characteristic of a mechanical prosthetic valve. (3:347)
167. (D) It is significantly decreased. The M-mode demonstrates a dilated and hypokinetic left ventricle. The markedly increased E point-to-septal separation is consistent with a decreased left ventricular ejection fraction. (23:140)
168. (B) Left ventricular end-diastolic pressure is increased. There is a mitral valve B notch, which is consistent with high end-diastolic pressure in the left ventricle. (24:69)
169. (A) Aortic stenosis and aortic insufficiency. The systolic waveform below baseline is consistent with moderate aortic stenosis. A mitral regurgitation waveform would be wider and is usually of higher velocity. The diastolic waveform above baseline is too high a velocity to be caused by mitral or tricuspid stenosis and is consistent with aortic insufficiency. (6:78)
170. (D) Coronary artery disease. The interventricular septum is hypokinetic and more echogenic than the posterior left ventricular wall. These findings are consistent with an old myocardial infarction. (1:478)
171. (C) Chordae tendineae. The M-mode cursor in this long-axis view is directed beyond the tips of the mitral leaflets at the level of the chordae tendineae—the level at which left ventricular measurements are obtained. (11:12)
172. (C) Caused by stagnant blood. The cloud of fuzzy smokelike echoes in the left ventricle is the result of blood stasis. It is usually seen when there is a severe decrease in left ventricular contractibility. (1:492)
173–179. If you are having a difficult time orienting yourself to an echocardiographic image, find a structure that is easy for you to recognize and work your way from there. For example, if you can identify the aortic root, you can then follow the anterior wall of the root as it continues into the interventricular septum. The posterior wall of the root will follow into the anterior mitral leaflet, and so on. 173. Right ventricle. 174. Aortic root. 175. Left atrium. 176. Descending aorta. 177. Left ventricle. 178. Pericardial effusion. 179. Pleural effusion. (1:558)
180. (D) A large pericardial effusion. A massive circumferential pericardial effusion is demonstrated in this fourchamber view. (11:253)
181. (B) Right ventricular wall. The presence of tamponade should be ruled out in patients with pericardial effusion, especially a massive one. A fairly specific echocardiographic sign of tamponade is diastolic collapse of the right ventricle, the right atrium, or both. (25:561)
182. (B) A diastolic jet filling the left ventricular outflow tract and extending deep into the left ventricle. This long-axis view demonstrates a flail right coronary cusp of the aortic valve. The cusp is seen extending into the left ventricular outflow tract in diastole. Color Doppler would be likely to demonstrate severe aortic insufficiency, which choice B describes. (12:100)
183. (D) The origin of the right coronary artery. With slight superior angulation from a standard short-axis view of the aortic valve, the ostia and proximal segments of the right coronary artery can be visualized. (11:23)
184. (B) False. The right ventricular outflow tract is located lateral to the origin of the right coronary artery. (1:102)
185. (A) Left-to-right shunting at the atrial level. There is a washout effect in the right atrium as blood from the left side of the heart enters the contrast-filled right atrium. (11:355)
186. (B) False. A pericardial effusion would appear on a subcostal four-chamber view as an echo-free space anterior to the right ventricle. (11:251)
187. (B) Liver parenchyma. To obtain a subcostal four-chamber view, the transducer is placed on the abdomen and angled in a cephalic direction. Therefore, liver parenchyma will occupy the near field of the image. (3:129)
188. (D) Pulmonary hypertension. An absent A wave and midsystolic notching (flying W sign) are consistent with this condition. (3:388)
189. (C) Mitral valve prolapse. The M-mode in Fig. 2–25 demonstrates late-systolic tricuspid valve prolapse. Tricuspid valve prolapse almost always occurs in patients with concomitant mitral valve prolapse. (1:305)
190. (C) Midsystolic notching. Fig. 2–26 is an example of systolic anterior motion of the mitral valve. This is one classic echocardiographic sign of hypertrophic obstructive cardiomyopathy. The midsystolic obstruction of the left ventricular outflow tract will often be demonstrated on the M-mode of the aortic valve as well as by midsystolic notching. (26:6)
191. (C) A dilated aortic root. This patient exhibits characteristic findings of Marfan syndrome, a connective tissue disorder. There is a linear echo near the aortic valve suggesting aortic root dissection, another complication of Marfan syndrome. This syndrome often causes ascending aortic dilatation as well as myxomatous degeneration of the aortic and mitral valves. (11:242)
192. (A) The long-axis suprasternal view. Because the aortic root is dilated, echocardiographic evaluation should follow the length of the aorta to determine the extent of the aneurysm. The suprasternal long-axis view allows for visualization of the aortic arch and the proximal portion of the descending aorta. Further investigation should include a modified apical two-chamber view for evaluating the thoracic aorta and a subcostal approach for interrogating the abdominal aorta. (3:121, 137)
193. (C) A large apical thrombus. This thrombus is seen filling the apex, with a piece of the medial segment protruding into the left ventricle. Most thrombi are associated with anterior infarctions and are located in the apex in the majority of cases. (1:489)
194. (B) It is flail. The tip of the posterior leaflet can be seen protruding into the left atrium, which is consistent with a flail mitral valve. (27:1383)
195. (B) Right pulmonary artery. The artery is seen in its short axis. (11:36)
196. (A) The left atrium. This atrium can sometimes be visualized posterior to the right pulmonary artery on the suprasternal long-axis view. (11:36)
197. (D) The moderator band. This is a muscular strip located in the apical third of the right ventricle. It is sometimes misdiagnosed as a right ventricular apical thrombus. (3:117, 294)
198. (B) A left atrial thrombus. This is seen protruding into the left atrium. (The bright linear echo in the right atrium originates from a pacemaker wire.) (1:592)
199. (B) Aortic stenosis, a calcified mitral annulus, and basal septal hypertrophy. The aortic valve is markedly calcified; there is a bright echo posterior to the mitral valve, representing a calcified mitral annulus; and the base of the interventricular septum is hypertrophied. The posterior echo-free space represents pleural effusion, as opposed to a pericardial effusion, because it does not taper at the descending aorta. (1:345, 283)
200. (D) An aged heart. When seen together, these findings usually indicate signs of aging. (9:1658)
201. (D) Atrial fibrillation. The electrocardiogram at the top of the Doppler tracing indicates this fibrillation. The variations from beat to beat reflect the altering lengths in diastolic filling periods that occur with atrial fibrillation. (11:333)
202. (B) Diastolic doming. The mitral valve is bulging into the left ventricle in diastole because the valve is stenotic and cannot accommodate all the blood available for delivery into the left ventricle. (1:251)
203. (A) The left atrium. Even without using the centimeter markers as a gauge, one can determine that the left atrium is dilated. In the long-axis view, the aortic root and left aorta should be approximately the same size. The apical four-chamber view is extremely useful for assessing relative chamber size. The right and left atria should be roughly the same size (although the left atrium is usually slightly larger), and they should be smaller than the ventricles. (11:368)
204. (D) An opening snap. The opening snap often affords the first clue to the diagnosis of mitral stenosis. (20:185)
205. (C) Descending aorta. A portion of the aorta can be seen lying behind the left atrium on the apical four-chamber view. (1:98)
206. (A) The mitral valve area. The pressure half-time, or the time it takes for the initial pressure drop of the mitral valve to be halved, can be used to measure the mitral valve area. A pressure half-time of 220 ms has been shown to correlate with a valve area of 1 cm2. (18:117)
207. (C) Left ventricular hypertrophy. The left ventricular walls are thickened and exhibit increased echogenicity. (28:188)
208. (B) A thickened mitral valve, a prominent interatrial septum, a small left ventricle, and pericardial effusion. The mitral valve and interatrial septum are slightly thickened, there is a small-to-moderate-sized pericardial effusion, and the left ventricle is small. (1:535)
209. (D) Amyloid cardiomyopathy. This patient exhibits classic features of this disease. The infiltrative process of the disease causes thickening of the ventricles, interatrial septum and valves. Pericardial effusion is another finding sometimes associated with this disease. (3:232)
210. (B) An endomyocardial biopsy. This has been shown to be helpful in identifying amyloid cardiomyopathy. (3:232)
211. (B) Ventricular septal defect. The short-axis and modified four-chamber views demonstrate a gap in the posterior aspect of the midsection of the interventricular septum. Given the patient’s history and the irregular borders on the echocardiogram, one can assume that this defect is acquired rather than congenital. (29:506)
212. (A) Color-flow Doppler imaging. This is particularly useful for quickly determining the location and quantifying the extent of abnormal blood flow in patients with ventricular septal defects. (3:243)
213. (A) Coronary sinus. When imaged from the apical two-chamber view, the coronary sinus appears as a circular structure in the atrioventricular groove. By rotating to a four-chamber view and angling posteriorly, one can follow the coronary sinus as it courses along the length of the posterior atrioventricular groove. (20:29)
214. (B) Deoxygenated blood. The coronary sinus carries venous blood to the right atrium. (30:211)
215. (A) Anteriorly. By tilting the scan plane anteriorly from this posteriorly directed apical four-chamber view, the aorta and left ventricular outflow tract can be imaged. (3:131)
216. (C) Prolapse of the posterior leaflet. The posterior mitral leaflet bulges beyond the plane of the mitral annulus, which is consistent with prolapse. (3:189)
217. (A) A systolic curve below baseline >3 m/s. Mitral valve prolapse, especially to the degree shown in this study, is most likely to be accompanied by some degree of mitral regurgitation, which is detected from the apical window with Doppler echocardiography by noting a systolic curve below baseline usually >3 m/s. (6:74)
218. (B) False. The arrow is pointing to the lateral wall of the left ventricle. (11:25)
219. (C) Artifactual. A dropout of echoes in the interatrial septum is not an uncommon finding when visualized from the apical four-chamber view. If this were a true atrial septal defect, a T sign would likely be noted. (1:404)
220. (A) Slight thickening of the valve with a normal opening. This thickening is noted best in diastole. The leaflets appear to open widely in systole. (They open in close proximity to the walls of the aortic root.) (1:279)
221. (C) 36 mm Hg. Using the simplified Bernoulli equation, the peak aortic gradient can be obtained by squaring the peak velocity (in this case 3 m/s) and then multiplying by 4. (18:23)
222. (B) Congenital aortic stenosis. In this disorder, the valve may be thin or minimally thickened, and M-mode may demonstrate a normal opening if the cursor was directed at the body of the leaflets rather than at the restricted tips. The best way to determine if congenital aortic stenosis is present is by noting Doppler evidence of increased velocities across the valve. (1:384)
223. (A) Systolic doming. This occurs in congenital aortic stenosis because the body of the leaflets expands to accommodate systolic flow while the tips of the leaflets restrict blood flow. (Normally, the tips of the aortic valve open wide and lie parallel to the aortic root in systole.) (1:383)
224. (C) It is exhibiting shaggy irregular echoes. The mitral valve has a mass of shaggy echoes with irregular borders attached to it. (3:277)
225. (B) Subacute bacterial endocarditis. Because of the patient’s history and the echocardiographic demonstration of an irregular mass attached to the mitral valve, this is the most likely diagnosis. (20:1141)
226. (B) Increased. Unlike calcium, which tends to inhibit valve opening, vegetations are likely to increase valve excursion. Because calcium and vegetations can look similar, echocardiographically this difference can aid in the diagnosis. (3:277)
227. (A) Systolic waveform below baseline. A mitral valve vegetation will usually cause the mitral valve to be regurgitant. Mitral regurgitation can be detected by continuouswave Doppler from the apical four-chamber view by noting systolic flow below baseline. (6:74)
228. (D) It prolapses into the left atrium and left ventricle. In Fig. 2–38A, the mass is in the left atrium. In Fig. 2–38B and C, the mass appears in the left ventricle. Therefore, one could deduce that the mass is prolapsing into the left atrium in systole and into the left ventricle in diastole. (1:312)
229. (B) The posteromedial papillary muscle. On the opposite wall of the left ventricle, one can see the anterolateral papillary muscle. Between the two papillary muscles, the tip of the mitral valve vegetation can be seen protruding into the left ventricle. (3:113)
1. Feigenbaum H. Echocardiography. 4th ed. Philadelphia: Lea & Febiger; 1986.
2. Henry WL, DeMaria A, Gramik R. Nomenclature and Standardization in Two-Dimensional Echocardiography. Raleigh, NC: American Society of Echocardiography; 1980.
3. Craig M. Diagnostic Medical Sonography: A Guide to Clinical Practice. Vol. 2. Echocardiography. Philadelphia: JB Lippincott; 1991.
4. Cosgrove DO, McCready VR. Ultrasound Imaging: Liver, Spleen, Pancreas. New York: John Wiley & Sons; 1982.
5. Weyman AE. Cross-Sectional Echocardiography. Philadelphia: Lea & Febiger; 1982.
6. Kisslo J, Adams D, Mark DB. Basic Doppler Echocardiography. New York: Churchill Livingstone; 1986.
7. Sahn DJ, DeMaria A, Kisso J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation. 1978; 58:1072-1083.
8. Sokolow M, McIlroy MB, Cheitlin MD. Clinical Cardiology. 5th ed. Norwalk, CT: Appleton & Lange; 1990.
9. Braunwald E. Heart Disease: A Textbook of Cardiovascular Medicine. 3rd ed. Philadelphia: WB Saunders; 1988.
10. Goldberg SJ, Allen HD, Marx GR, Flinn CJ. Doppler Echocardiography. Philadelphia: Lea & Febiger; 1985.
11. Harrigan P, Lee R. Principles of Interpretation in Echocardiography. New York: John Wiley & Sons; 1985.
12. Kisso J, Adams DB, Belkin RN. Doppler Color-Flow Imaging. New York: Churchill Livingstone; 1988.
13. Salcedo E. Atlas of Echocardiography. 2nd ed. Philadelphia: WB Saunders; 1985.
14. Hatle L, Angelsen B, Tromsdal A. Noninvasive assessment of atrio-ventricular pressure half-time by Doppler ultrasound. Circulation. 1979; 60:1096-1104.
15. Gravanis MB. Cardiovascular Pathophysiology. New York: McGraw-Hill; 1987.
16. Popp RL. Echocardiography. N Engl J Med. 1990; 323:101-109.
17. Aobanu J, et al. Pulsed Doppler echocardiography in the diagnosis and estimation of severity of aortic insufficiency. Am J Cardiol. 1982; 49:339-343.
18. Hatle L, Angelsen B. Doppler Ultrasound in Cardiology: Physical Principles and Clinical Applications. Philadelphia: Lea & Febiger; 1985.
19. Currie PJ. Transesophageal echocardiography: new window to the heart. Circulation. 1989; 80:215-218.
20. Hurst JW. The Heart, 6th ed. New York: McGraw-Hill; 1986.
21. Wasser HJ, Greengart A, et al. Echocardiographic assessment of posterior left ventricular aneurysms. J Diagn Med Sonography. 1986; 2:93-95.
22. Driscoll DJ, Fuster V, McGoon DC. Congenital heart disease in adolescents and adults: atrioventricular canal defect. In: Brandenburg RO, Fuster V, Giulani ER, et al., eds. Cardiology: Fundamentals and Practice. Chicago: Year Book Medical Publishers; 1987.
23. D’Cruz IA, Lalmalani GG, et al. The superiority of mitral E pointventricular septum separation to other echocardiographic indicators of left ventricular performance. Clin Cardiol. 1979; 2:140.
24. D’Cruz IA, Kleinman D, Aboulatta H, et al. A reappraisal of the mitral B-bump (B-inflection): its relationship to left ventricular dysfunction. Echocardiography. 1990; 7:69-75.
25. Williams GJ, Partidge JB, Right ventricular diastolic collapse: an echocardiographic sign of tamponade. Br Heart J. 1983; 49:292.
26. Doi YL, McKenna WJ, et al. M-mode echocardiography in hypertrophic cardiomyopathy: diagnostic criteria and prediction of obstruction. Am J Cardiol. 1980; 45:6-14.
27. Child JS, Skorton DJ, Taylor RD, et al. M-mode and cross-sectional echocardiographic features of flail posterior mitral leaflets. Am J Cardiol. 1979; 44:1383-1390.
28. Sigueira-Filho AG, Cunha CL, Tajik AJ, et al. M-mode and two-dimensional echocardiographic features in cardiac amyloidosis. Circulation. 1981; 63:188-196.
29. Chandraratna PAN, Balachandran PK, Shah PM, Hodges M. Echocardiographic observations on ventricular septal rupture complicating myocardial infarction. Circulation. 1975; 51:506-510.
30. Berne RM, Levy MN. Cardiovascular Physiology. 4th ed. St. Louis: CV Mosby; 1981.
31. Allen MN. Diagnostic Medical Sonography: A Guide to Clinical Practice Echocardiography. 2nd ed. Philadelphia: Lippincott; 1999.
* This chapter is reprinted from the third edition of Appleton & Lange Review for the Ultrasonography Examination.