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Ebook Clinical manual and review of transesophageal echocardiography (2nd edition): Part 2

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(BQ) Part 2 book Clinical manual and review of transesophageal echocardiography presents the following contents: Clinical perioperative echocardiography, transesophageal echocardiography in nonoperative settings, special topics, appendices.

PERICARDIAL D I S EASES 45 Properties of the parietal pericardium include: a Collagen fibers meshed with elastic fibers b Flexibility c Rigidity in older patients d Lining of the fibrous pericardium e All of the above 46 The inflammatory phase of pericarditis is marked by all of the following except a Infiltration with leukocytes such as lymphocytes, polymorphonuclear leukocytes, and macrophages b Alterations in pericardia! vascularity c Deposition of fibrin d Decrease in pericardia! fluid content 47 In patients over 60 years of age, the D wave of pul­ monary vein flow Doppler examination is generally greater in magnitude than the S wave I 369 a True b False 48 In constrictive pericarditis, the thickened pericardium isolates the intrapericardial cardiac chambers (but not the extrapericardially located pulmonary veins) from changes in intrathoracic pressure during the respira­ tory cycle a True b False 49 Prominent hepatic vein diastolic flow reversal may be noticed as a result of increased RA pressure only in patients with significant tricuspid regurgitation and sinus tachycardia a True b False Ec h oca rd i og p hy fo r Ao rti c S u rg e ry Christopher Hudson, Jose Coddens, and Madhav Swaminathan INTRODUCTION Diseases involving the aorta can present a challenge to both surgeons and anesthesiologists Aortic dissection and rupture are life threatening, require rapid and accu­ rate diagnosis, and need definitive medical and/or sur­ gical management due to their high risk of morbidity and mortality •2 A key ingredient in the efficient man­ agement of these patients is imaging of the thoracic aorta Transesophageal echocardiography (TEE) has become an essential noninvasive diagnostic modality for acute thoracic aortic pathologies, and is a standard part of the echocardiographer's armamentarium in the oper­ ating room 3-6 It is important for the echocardiographer to quickly and accurately verifY the diagnosis, distinguish true pathology &om the many common confounding artifacts, and clearly communicate precise echocardio­ graphic findings of the aorta and related cardiac anatomy to the surgeon in order to guide intervention The follow­ ing text reviews aortic anatomy and pathology and associ­ ated echocardiographic features that assist with imaging during aortic surgery ANATOMY OF THE AORTA In order to truly appreciate the invaluable role that TEE plays in the assessment for diseases of the aorta, a detailed understanding of the aorta and surrounding anatomic structures is crucial The thoracic aorta can be divided into three anatomic segments: ascending thoracic aorta, aortic arch, and descending thoracic aorta (Figure 6- ) The ascending thoracic aorta orig­ inates at the level of the aortic valve annulus As previ­ ously described in Chapter 9, the aortic valve com­ prises three crescent-shaped leaflets that coapt to form three commissures Immediately distal to the aortic valve apparatus is a short and dilated aortic segment­ the sinus of Valsalva-which is subdivided into the noncoronary, left coronary, and right coronary sinuses As the nomenclature suggests, the left and right coro­ nary arteries each originate from their respectively named sinus Distal to the sinus of Valsalva, the aorta slightly narrows, forming the sinotubular j unction (STJ) From this point, the ascending aorta crosses beneath the main pulmonary artery, then courses in an anterior, cranial, and rightward direction over the ori­ gin of the right pulmonary artery The ascending aorta terminates and continues as the aortic arch at the origin of the brachiocephalic (innomi­ nate) artery The aortic arch then proceeds to curve in a posterior and leftward direction with cranial convexity Three arteries arise from the aortic arch: the brachia­ cephalic, left common carotid, and left subclavian arter­ ies It is often difficult to visualize the distal ascending thoracic aorta and proximal aortic arch with TEE because the trachea is positioned between the esophagus and aorta, effectively preventing ultrasound transmission Immediately beyond the origin of the left subclavian artery, at the point of attachment of ligamentum arteria­ sum (remnant of the fetal ductus arteriosus), is a second narrowing called the aortic isthmus Unlike the heart and proximal part of the aorta, the aortic isthmus and descending thoracic aorta are relatively fixed Conse­ quently, deceleration inj ury secondary to trauma is most often confined to this level Distal to the aortic isthmus, the descending aorta follows a caudal, slightly anterior, and rightward trajectory towards the aortic diaphragmatic hiatus Along its intrathoracic course, the descending thoracic aorta and the esophagus are in close proximity While the esophagus courses almost straight downward, anterior to the midline of the ver­ tebral bodies, the aorta travels in a smooth, curved direction from the anterolateral side of the 4th thoracic vertebral body to the anterior side of the 1 th vertebral body During its thoracic descent, multiple intercostal arteries branch off the aorta and may occasionally be imaged with TEE using color-flow Doppler (CFD) Spinal branches of these intercostal arteries supply blood to the spinal cord through radicular arteries The radicular artery anatomy in this area is quite variable, with to radicular branches typically contributing to the thoracic spinal cord The anterior spinal cord blood supply is tenuous in the thoracic region, thus it is ECHOCARDIOGRAPHY FOR AORTIC SU RGERY Trachea Brachiocephalic a Subclavian a I 37 left and right sides of the aorta, slightly below the mesenteric vessels The wall of the aorta is composed of three tunicae: the intima, media, and adventia The inner layer, the intima, consists of simple squamous epithelium and underlying connective tissue The tunica media consists of circularly arranged smooth muscle and elastic tissue The outer adventitial layer is mainly a loose layer of con­ nective tissue, lymphatics, and vasa vasorum (ie, "vessels of the vessels") TEE provides the ability to assess the aor­ tic wall for many pathologies including thickening of the tunica intima due to arteriosclerosis and/or atherosclero­ sis, intimal tears/dissections, and aneurysmal dilatation ECHOCARDIOGRAP HIC EVALUATION OF THE THORACIC AORTA FIGURE 6- Anatomic cou rse of the thoracic aorta The relations h i p with the esophagus is particularly i m portant with regard to orientation of the probe and the aorta i n each of its thoracic sections: the ascending aorta, aortic arch, and descending aorta The i nterposi­ tion of the trachea makes portions of the ascending aorta and arch either completely invisible or partially visible at great risk for cord ischemia Frequently, one radicular artery-the arteria radicularis magna, or the artery of Adamkiewicz-is very developed and is responsible for the majority of anterior spinal cord blood supply, and it is typically found between T9 and T l Below the diaphragm, the abdominal aorta lies posterior to the stomach Because the stomach is a large cavity that is highly deformable, the position of the abdominal aorta in relation to the intragastric TEE probe is somewhat variable The celiac artery and mesenteric arteries originate from the anterior side of the abdominal aorta The renal arteries arise from the As described in Chapter , insertion of the TEE probe must be performed gently and should never be forced through areas of resistance This is especially important in patients with suspicion of major aortic pathology First, intubation of the esophagus with the TEE probe can be very stimulating and may result in hypertensive episodes, increasing the risk of further tearing or rup­ ture of a dissection or aneurysm Second, resistance encountered during advancement of the probe may rep­ resent esophageal compression by a large aneurysm, and if so, consideration should be given to abandon the examination Finally, in aortic dissection, because the adventitia is the sole layer of the wall of the false lumen, aortic rupture may occur if the TEE probe is not manipulated cautiously As with any TEE examination, a systematic approach is required to thoroughly evaluate the thoracic aorta As per the SCA/ASE guidelines, there are six short-axis and two long-axis imaging planes that enable imaging of most of the thoracic aorta? Although many sequences are possible, the authors recommend the following order: Begin with the midesophageal (ME) aortic valve (AV) short-axis (SAX) , "Mercedes-Benz'' view, which is obtained at the midesophageal level with the scan angle rotated forward to 30° to 60° (see Figure 5-1 9B) From here, the angle can be rotated by another 90° to about 20° to 50° to identify the ME AV long-axis (LAX) view (see Figure 5-20B) The long-axis view is particu­ larly important because it allows evaluation of the aortic valve and proximal ascending aorta Measurements can be made of the left ventricular outflow tract (LVOT), aor­ tic valve annulus, sinuses of Valsalva, STJ, and ascending aorta if aortic valve repair and/or root reconstruction are planned (Figure 6-2) In order to visualize the ascend­ ing aorta in short axis, rotate back to a scan angle of 0° and slowly withdraw from the level of the aortic valve (ie, ME ascending aorta SAX view; see Figure 5-30B) By rotating forward to a 20° scan angle, a ME ascending 372 C H A PTER A B FIGURE 6-2 Midesophageal aortic va lve long-axis view shown as a mid-systolic frame (panel A) and with rele­ vant measurements (pa nel B) See text for deta i ls.(AV, aortic va lve; LVOT, left ventricular outflow tract) aorta LAX view is obtained (see Figure 5-32B) It is crucial in these two views to carefully examine the aorta for dissections Artifacts are frequently encountered within the ascending aorta, and it is important to dis­ tinguish artifacts from true pathology as discussed in Chapter Following examination o f the ascending aorta, the TEE probe should be advanced to the level of the ME four-chamber view and rotated towards the patient's left This should result in the descending aorta SAX view in which the aorta appears as a circular image at the top of the screen (Figure 6-3) AB the descending aorta is about to em in diameter at this level, reduc­ ing the scan depth to to em and selecting a high transducer frequency improves both the spatial and temporal resolutions of the image Almost the entire descending thoracic aorta may be visualized in short axis by advancing and withdrawing the TEE probe By rotating the scan angle forward to 90°, the descending aorta can be seen longitudinally (see Figure 6-3) FIGURE 6-3 Short- (left) and long-axis (right) views of the descending aorta shown simu lta neously with x-plane imaging ECHOCARDIOGRAPHY FOR AORTIC SU RGERY Alternating between short- and long-axis views may help demonstrate aortic pathology more comprehen­ sively While withdrawing the TEE probe and main­ taining the descending aorta in the short-axis view (at 0°) , the aorta will change in appearance from circu­ lar to longitudinal at the level of the aortic arch (upper esophageal [UE] aortic arch LAX; see Figure 5-34) Frequently, the origins of the left subclavian and carotid arteries can be seen Adding CFD with the Nyquist limit set at 50 cm/s may aid in visualizing these vessels Finally, by rotating forward to 90°, the UE aortic arch SAX will be obtained (see Figure 5-3 B) Most aortic pathologies can be identified by adding pulsed-wave Doppler (PWD) and continuous-wave Doppler (CWD), as well as gray-scale and color M-mode to the two­ dimensional (2D) examination above AORTIC ANEURYSMS An aortic aneurysm is a localized or diffuse dilation of the aorta to twice its diameter involving all three layers of the vessel wall The estimated annual incidence is six cases per 00,000 persons TEE is useful for the diag­ nosis and classification of thoracic and upper abdomi­ nal aortic aneurysms Thoracoadominal aneurysms (TAAs) are categorized into four types based on the Crawford classification system (Figure 6-4) Type I involves the entire descending thoracic aorta to the abdominal aorta above the renal arteries Type II origi­ nates in the proximal descending thoracic aorta and ter­ minates distal to the renal arteries Type III affects the distal half of the thoracic aorta and the abdominal aorta to the bifurcation Type IV is limited to the distal por­ tion of the descending thoracic aorta and the abdomi­ nal aorta to the bifurcation I 73 Aneurysms are generally thought to be a disease of aging and a consequence of degeneration and athero­ sclerosis Aging results in a pathological process that involves the development of eccentric fibrous intimal thickening, lipid deposition, and calcification, leading to weakening of the aortic wall and dilation Accord­ ing to Laplace law (Tension = Pressure X Radius), as the diameter of the lumen increases, the wall tension increases resulting in progressive dilation Other causes ofTAAs include connective tissue diseases (ie, Marfan's, type IV Ehlers-Danlos and Loeys-Dietz syndromes) , infections (ie, bacteria, mycotic, or syphilitic) , trauma, and increased wall tension secondary to hypertension or a high-velocity jet originating from aortic stenosis The decision to surgically repair a TM is based upon the size and etiology of the aneurysm According to recommendations by the Society of Thoracic Surgeons, a thoracic fusiform aneurysm should be surgically repaired if it is greater than em in diameter or twice the diameter of the normal contiguous aorta 1 Indications for saccular aneurysm have not been deter­ mined, but it is considered reasonable to intervene if the width is greater than em Patients with connective tissue diseases, such as Marfan's syndrome, may be con­ sidered for early operative repair because of their increased risk of dissection or rupture A strong family history of aortic aneuryms may also prompt early inter­ vention Finally, symptomatic patients should be considered for operative treatment regardless of the size of the aneurysm Symptoms include persistent pain, malperfusion, and compression of nearby structures leading to dysphagia, cough, hoarseness, or Horner's syndrome Descending TAAs can also be treated by endovascular stent grafting There are no established guidelines regarding which patients should be managed D i ssect i o n s FIGURE 6-4 Classifica­ tion of aortic d issection and aneurysms D e Bakey Type I Type II Stanrord Type A Type Il Type B Crawlord Type I crawrord Type II Crawlord Type Ill crawrord Type IV 74 C H A PTER with endovascular aortic repair (EVAR) In general, patients at high risk for complications from either con­ ventional open repair or medical management may bene­ fit from this relatively less invasive approach Another emerging alternative for complex aortic pathology is the "hybrid" approach in which an open surgical technique is combined with an EVAR This approach is thought to maximize the benefit of complete repair of com­ plex lesions while minimizing the risk of a total open technique TEE may be used to detect the patency of aortic side branches and to evaluate for the presence of organ malperfusion In the thoracic region, the identification of the left subclavian artery and its patency may be par­ ticularly important in EVAR and hybrid approaches Intraoperative TEE is also an excellent monitoring tool, especially if aortic cross-clamping is performed, and may be helpful during cannulation if total or partial extracorporeal circulatory support is required Monitor­ ing of cardiac function is an added benefit of TEE dur­ ing aortic aneurysm surgery While the aorta remains the focus of intraoperative imaging, the effects of aortic manipulation on cardiac function can also be evaluated This enables clinicians to make informed decisions on pharmacological support, should it be required AORTIC DISSECTION An aortic dissection is a separation in the aortic wall that allows blood flow within the tunica media Cur­ rently, there are two proposed etiologies for aortic dis­ sections In the first hypothesis, the intima is rup­ tured along the edge of an atheromatous plaque or at a penetrating ulcer The high pressure in the aorta forces blood through the intimal tear into the tunica media, creating a false lumen The intimal layer that separates the false lumen from the true lumen (normal conduit of blood in the aorta) is termed the intimal flap While intimal injury per se does not lead to dissection, it is a common precipitating factor, especially when the aortic medial layer is diseased In the second hypothesis, the dissection is attributed to spontaneous rupture of the vasa vasorum or degeneration of the collagen and elastin that make up the tunica media This medial layer can be affected by poor structural integrity as seen in old age or with primary connective tissue diseases such as Marfan's syndrome Apart from medial integrity, the time required for extension of an intimal tear and development of a dissection depends on the rate of rise of systolic pressure, pulsatile pressure, dias­ tolic recoil, and mean arterial pressure Aortic dissection is the most common cause of death among all conditions involving the aorta The incidence of thoracic aortic dissection in North America is about to cases per million people per year The mortality associated with acute aortic dissection is extremely high, with % of patients dying before hospital admission 14 The mortality rate from acute aortic dissection has been shown to be o/o to 3% per hour for the first 24 to 48 hours, and as high as 80% by weeks Due to this high mortality, early diagnosis is considered crucial for appropriate management to be initiated Magnetic resonance imaging (MRI) is currently the gold standard test for the detection and assessment of aor­ tic dissections with a sensitivity and specificity of 98% and 98%, respectively 16 However, there are many contraindi­ cations to MRI examination including implanted medical devices (ie, pacemaker, orthopedic hardware, etc) and hemodynamic instability Consequently, TEE is increas­ ingly becoming an important and convenient modality for diagnosis of acute aortic dissection TEE, similar to MRI, is highly sensitive and specific for the diagnosis of aortic dissection, with a sensitivity of 97% and specificity of 00% TEE is an attractive first-choice diagnostic proce­ dure because of its accuracy, speed, relatively low cost, portability, and noninvasiveness 18 However, a major limitation ofTEE in the diagnosis of aortic dissection is the inability to reliably visualize the distal ascending aorta and proximal aortic arch The frequent presence of arti­ facts such as mirror images in aortic imaging makes TEE prone to important false-positive diagnoses of dissection (Figure 6-5) There are two main classification systems utilized for thoracic aortic dissections (see Figure 6-4) The DeBakey classification system recognizes three types of aortic dissections 9•20 In type I, the entire aorta is dis­ sected; in type II, only the ascending aorta is involved; and in type III, the ascending aorta and arch are spared, while the descending aorta is dissected Type III is fur­ ther subclassified into type IliA, involving the descend­ ing thoracic aorta alone, and type IIIB, extending into the abdominal aorta The Stanford system classifies dis­ sections into two types 20 In Type A the ascending aorta is affected, while in Type B the ascending aorta is spared A classification system from Europe has also been proposed to replace the DeBakey and Stanford classification systems •22 This classification groups dis­ section into five types based on etiology (Table 6- ) These classification systems have important prognos­ tic and therapeutic consequences 1 •23 Type A aortic dis­ section is a formal indication for surgical intervention because the reported mortality rate with medical therapy far exceeds that reported for surgical treatment 24-26 Unlike Type A aortic dissections, the correct manage­ ment for Type B aortic dissections remains controver­ sial 27-29 Medical management is advocated for most Type B dissections as most studies show no clear survival advantage with surgical management Some indications for surgery in Type B dissection include organ malper­ fusion, persistent pain, hemodynamic instability, or ECHOCARDIOGRAPHY FOR AORTIC SU RGERY I 375 FIGURE 6-5 Mides­ ophagea l ascending aortic long-axis view with a suspi­ cious shadow (?) in the aortic l u men The pul monary a rtery (PA) catheter may cast a m ir­ ror image artifact in the ascending aorta that d isplays a similar"bou nce"to that of an intimal flap, creating a n i m pression o f a dissection Similarly, a n actua l dissection flap may be erroneously m is­ taken for an artifact any signs of impending or ongoing rupture, notably the accumulation of pleural, pericardia!, periaortic, or mediastinal fluid; propagation of the dissection; increasing size of hematoma; and development of a saccular aneurysm In addition, echocardiographic evi­ dence of a wide-open false lumen with communication to the true lumen increases the risk of progression of the dissection, and therefore is considered an indica­ tion for surgery Though an intimal tear is the classic finding for aor­ tic dissection, it is not always present The presence of an intimal flap is therefore considered a classical sign of dissection, but not a mandatory one The TEE exami­ nation of a patient with aortic dissection involves sev­ eral components including characterization of the dis­ section, assessment of flow in aortic branches, and determination of cardiac complications The dissection flap is a thin, mobile echogenic membrane found within Table 6- E u ropea n Society of Card i o logy C l assification of Aortic D i s sectio ns Class I II Ill IV V Description Classic aortic dissection (DeBakey and Stanford) I ntramural hematoma/hemorrhage Discrete/subtle dissection without hematoma Plaque rupture leading to aortic ulceration Traumatic or iatrogenic the aortic lumen; however, t o avoid a false-positive diagnosis, the intimal flap must be identified in multi­ ple image planes 8·30 ,3I Although identification of the site of the intimal tear can be challenging, CFD imag­ ing is useful in the assessment of entry and exit sites It can sometimes be very difficult to distinguish the true lumen from the false lumen In contrast to the false lumen, the true lumen tends to be smaller, round in appearance, shows enlargement during systole, and often has normal PWD and CFD profiles In addition, M-mode imaging can help determine the direction of movement of the flap in systole, and thereby identify the location of the true lumen (Figure 6-6) The false lumen is usually larger and crescent shaped, and often demonstrates spontaneous echo contrast suggesting sluggish blood flow Closure of the tear to prevent further spread of the dissection is an essential part of the surgical repair 32 Ascending aortic dissection usually requires a formal sternotomy, while descending aortic dissections can be managed by open (thoracotomy) , EVAR, or hybrid techniques The two most common sites of intimal tear are to em above the sinuses of Valsalva (70%) and the ligamentum arteriosum (30%) 33-35 Other variants of aortic dissection include intra­ mural hematoma (IMH) and aortic ulcers Intramural hematoma (ie, European Heart Society class II dissec­ tion) is a common finding with a prevalence of up to 30% ·37 The false lumen is believed to be due to rupture of vasa vasorum in the tunica media resulting 76 C H A PTER Tech niq ues of determining flow i n the true l u men Pa nel (A) is a two-d imensional midesophageal long-axis view of the descending aorta showing two possible l u mens The appl ication of color-flow Doppler (panel 8) demonstrates higher velocity flow in the true l umen M-mode imaging across the long axis of the aorta (panel C) demonstrates the two sides of the true l u m e n expa nd in g in systo le as the intra l u m i n al pressure i ncreases Color M-mode imaging (panel D) shows color-flow signa ls within the true l u men i n systole corresponding with the expanding l u men in pa nel (C) FIGURE 6-6 in hematoma formation There are two distinctive types of IMH Type I IMH has a smooth intraluminal surface, a diameter less than 3.5 em, and a wall thick­ ness greater than em, while type II IMH has a rough intraluminal surface, a diameter greater than em, and a wall thickness greater than 0.6 em Both types have a longitudinal extension of at least 1 em Atherosclerotic aortic plaques can also ulcerate (ie, European Heart Society class IV dissection) leading to the formation of aneuryms, aortic rupture, or dissec­ tions 39 The ulcers predominantly affect the descending thoracic aorta and are not usually associated with longi­ tudinal extension On TEE, these lesions are characterized by a discrete ulcer penetrating the aortic wall with or without intramural hematoma While identification and characterization of the dissection remains extremely important, there are several other crucial aspects of the echocardiographic examination for a patient with aortic dissection Functional aortic insufficiency (AI) occurs frequently in patients with acute Type A aortic dissection, with approximately 44% being severe AI The mecha­ nisms of the AI include incomplete leaflet closure due to leaflet tethering in a dilated aorta, aortic leaflet prolapse due to disruption of leaflet attach­ ments, and dissection flap prolapse through the ECHOCARDIOGRAPHY FOR AORTIC SU RGERY aortic valve orifice The management of AI associ­ ated with aortic dissection is controversial If the aor­ tic valve leaflets are otherwise normal, preservation of the native valve can be achieved in up to 86% of Type A dissections.4o The aorta has several side branches, including the _ coronary artenes, cerebral vessels, celiac and mesenteric vessels, renal arteries, and spinal cord vessels, which can be compromised as a consequence of dissection The incidence of coronary artery involvement in aortic dis­ section can be as high as 0% to 20%.41 The left main �nd r!ght coronary arteries can often be reliably visual­ Ized m the ME AV SAX viewY Direct evidence of coronary involvement is the presence of a dissection flap_ exten�ing int? the ostium of the coronary vessel Indirect evidence mcludes electrocardiographic (ECG) changes, cardiovascular instability, and echocardio­ graphic findings of regional wall motion abnormalities Although branch arteries of the aortic arch can be reli­ ably visualized with TEE,42 43 the use of additional modalities including epiaortic scanning and surface Doppler directly over the carotid arteries to assess dis­ section extent into the arch vessels is highly recom­ mend�d 44 �he remaini�g side branches including the renal, mtestmal, and spmal cord vessels are more diffi­ cult to examine with TEE Other important echocardiographic findings include the presence of pericardia! and left pleural effusions Although peri�ardi� effusions can result from the rup­ ture of the dissection through the wall of the aortic root, the most common cause is from the transudation of fluid across the false lumen 4.45 The development of left pleural effusion is similar except for the fact that the rupture occurs in the descending thoracic aorta.46 , 47 A pericardia! effusion appears as an echolucent space between the parietal and visceral pericardium on TEE Echocardiographic signs suggesting tamponade include early diastolic collapse of the right ventricle, late dias­ tolic/early systolic collapse of the right or left atrium, decreased size of the cardiac chambers, and abnormal ventricular septal wall motion with inspiration A left pleural effusion is best seen in the descending aorta SAX view as an echolucent space that resembles a "claw" (Figure 6-7) Intraoperatively, TEE is a valuable tool to monitor volu �e status and global and regional left ventricular funcuon It can also assist with cannulation and discern whether the malperfused side branches originate from the false or the true lumen-information that is essen­ tial in the surgical decision to reimplant these vessels Finally, TEE can be used to evaluate the success of the surgical repair (ie, absence of blood flow in the false lumen) and assess for the presence of residual AI and resolution of wall motion abnormalities or pericardia! and pleural effusions I 377 FIGURE 6-7 Midesophageal short-axis view o f the descending aorta demonstrating a crescent-shaped echol ucent s pace that suggests a sig n ificant left pleural effusion AORTIC ATHEROSCL EROSIS Stroke continues to be a significant cause of morbidity and mortality after cardiac surgery Strokes occur in approximately 1% to 6% of patients following cardiac surgery and account for nearly 20% of deaths.48-50 The association between aortic atheromatous disease and stroke _ has been clearly defined.5 l-53 Techniques for detectmg the presence of aortic atheromas include manual palpation, x-ray, magnetic resonance and tomo­ graphic scans, and cardiac catheterization However, TEE and epiaortic ultrasound are generally considered to be superior imaging modalities.54.55 �everal classification systems for grading the severity of aortic a�eromas have been proposed A commonly used system IS that of Katz and colleagues who divided the severity of atherosclerosis into five grades (Table 6-2) 52 It should be noted, however, that these measurement and categorization schemes are limited because they Table 6-2 C l a ssification of th oracic a o rtic athero m a Grade Description Normal aorta Severe intimal thickening Atheroma protruding 5 mm into aortic lumen Mobile atheroma 78 C H A PTER measure only maximal thickness and not account for total plaque area (ie, "atheroma burden'') within any given segment of aorta Furthermore, the thickness measurement is just a one-dimensional estimate of a three-dimensional atherosclerotic lesion Another limitation of grading systems is that gray-scale density, calcification, surface texture, and ulceration are highly subjective atheroma char­ acteristics and prone to interobserver variability Irrespective of the specific classification system used, patients with advanced aortic atherosclerosis are at high risk for adverse outcomes-patients with grade lesions have a -year mortality rate of25%.525 Although TEE has been useful in diagnosing aortic atheromatous disease, it is not without limitations The usual site for aortic cannulation and cross-clamping during cardiopulmonary bypass is the distal ascending aorta and proximal arch, which are difficult areas to visualize with TEE.57·5 It is also believed that aortic manipulation may result in plaque embolism and sub­ sequent neurological injury 59 It is therefore possible to miss the presence of severe aortic disease with TEE alone Konstadt et al found that severe atherosclerosis in the ascending aorta was not detected in 9% of cases 57 Epiaortic ultrasound has been shown to overcome this limitation and has emerged as the gold standard for detecting the extent and distribution of ascending aortic atherosclerosis 44• 60 It is important to note that although it is possible to accurately detect atheromatous disease with a combination of TEE and epiaortic scanning, any subsequent alteration in surgical management has not been conclusively shown to reduce the incidence of neu­ rological sequelae 61 · 62 There are numerous surgical tech­ niques that focus on reducing the manipulation of the ascending aorta in an effort to decrease embolic events These include using alternate atheroma-free sites for can­ nulation, cross-damping, and placement of proximal anastomoses; deep hypothermic circulatory arrest for improved neurologic protection; off-pump approaches; and avoidance of cross-damping altogether 60 ,63 -66 AORTIC TRAUMA Traumatic aortic disease is associated with an exception­ ally high mortality 67· 68 The reported mortality rate of patients who present to the hospital with a traumatic aortic injury is about 30% Severe deceleration is the most common etiology, with the injury most commonly occurring at the aortic isthmus (approximately 54% to 67% of the time) 67 Other sites of injury, in order of decreasing frequency, are the descending thoracic aorta, the aortic arch, and the abdominal aorta Computed tomography (CT) scan and aortography remain the diagnostic imaging modalities of choice 69 However, these modalities can be time consuming, require trans­ port of a potentially unstable patient, and necessitate administration of nephrotoxic contrast agents In con­ trast, TEE, with a reported o/o sensitivity and 00% specificity, is noninvasive, can be performed at the bed­ side, and avoids the use of contrast agents, but may also be limited by availability of suitably trained personnel Three types of lesions may be encountered: a subad­ ventitial traumatic aortic rupture, a traumatic aortic inti­ mal tear, or a mediastinal hematoma The subadventitial traumatic aortic rupture may be partial, subtotal, or complete, and is characterized by the presence of blood flow on both sides of the disruption A flap consisting of intima and media can also be found There may be a disrupted aortic wall and a deformed aortic contour, although the aortic diameter is usually preserved It can sometimes be very difficult to differentiate subadventitial traumatic aortic rupture from aortic dissection Echocar­ diographic findings supporting subadventitial traumatic aortic rupture include asymmetrical contour at the level of aortic isthmus, thick and highly mobile medial flap, absence of tear, presence of mediastinal hematoma, simi­ lar blood flow velocities on both sides of the flap, and mosaic color Doppler flow surrounding the disruption In contrast, TEE findings supporting aortic dissection include symmetrical enlargement of the aortic contour, thin and less mobile intimal flap, entry and exit tears, no mediastinal hematoma, thrombus formation in the false lumen, different blood flow velocities in both the true and false lumens, and finally, absence of mosaic color Doppler flow mapping on both sides of the intimal flap Traumatic aortic intimal tears appear echocardio­ graphically as thin, mobile intraluminal appendages of aortic wall that are located in the region of the aortic isthmus Since these lesions are small and superficial, the contour and diameter are unaffected, and color­ flow mapping does not demonstrate turbulence Medi­ astinal hematomas have three characteristic TEE find­ ings: increasing space between the probe and the wall of the aorta, double contour aortic wall, and a distinct echogenic space between the bright aortic wall and the visceral pleura This space is typically seen in the far field adjacent to the posterolateral aortic wall Associated lesions with traumatic aortic injury have been reported by Goarin and colleagues.70 These consist of pulmonary contusion, left pleural effusion, rib fractures, diaphragmatic rupture, mediastinal hematoma, hemoperi­ cardium, myocardial contusion, valvular lesions, and hypovolemia Some of these lesions become apparent much later after the initial injury; hence, a follow-up TEE examination is mandatory ENDOVASCUL AR STENTING In the early 990s, the use of endovascular stems to treat aortic pathologies was introduced Since then, stents have become an increasingly utilized alternative to conventional I 628 A N SWERS b 18 b 1 b 19 12 d 20 b c b 14 d 22 d d 23 d 13 a c 24 c d 25 a I n d ex Page num bers followed by for t i ndicate figures or tables, respectively A Aortic aneurysm classification, 373, A mode, Abdom i n al aorta, 37 See also Aorta Abso rption, of sound waves, Acoustic i mpedance, Acoustic noise, 48 etiol ogies, 373 pathophysiology, Acoustic shadowing, 46, 47/ Acoustic variables, Afterload, 26 Alfieri stitch ("bow-tie" repai r), for m itral valve repair, ep i aortic ultrasonography, 80, 459, 460j 461/ reverberation artifact, 48/ tomographic views, 1 9j 1/ Aortic atherosclerosis 47 epiaortic ultrasonography, Amplitude, , 2/ Amyloidosis, 334-335, 335/ Anatomic variants, 36, 37j -52 See also specific structures Anesthesia i nduction, i n lung transplantation, 468 myocacdial contractil i ty and, 32-1 33 Aneurysm Anomalous pulmonary venous return, 408-409, 408j 409J Anteflexion, of probe, 88, 89f Anth racyclines, 336 Aorta anatomy, 370-37 , 37 1/ aneurys m See Aortic aneurysm arch See Aortic arch ascendi ng, tomographic views deep rransgastric long-axis, 375j 492j 494 pericardia! and pleural effusion i n , plaque rupture i n , 376 surgical repair, 374-375 377, 377/ i n emergency department, 492-493, 492/ intraoperative, 377 for location of true lumen, 375, 376j 493-494, midesophageal lo ng-axis view, pleural effusion, 77f 372/ atherosclerosis See Aortic atherosclerosis coarcration of, 380, 424-426, 426/ descen ding, tomographic views, 1 7, 1j 372-373, versus traumatic disruption, 497, disruption Aortic regurgitation aortic stenosis and, 3, 3t 493/ 49/ 497 t See also Aorta, traumatic aortic valve repair versus replacement for, 4-2 215 LVAD placement and, 395, 397 measurement, 68 m itral stenosi.s and, 3, 3t pathophysiology, 207 severity classification, 207-208, 208j 58 t, 582t catdioplegia delivery i n , 372/ dissection See Aortic dissection epiaortic ultrasonography, 46j 45 8-459, 459j 460/ root, 7t supravalvular obstruction, 424 three-dimensional echocardi ography, 1/ traumatic disruption versus aortic dissection, aortic insufficiency i n , 376-377 versus artifacts, on TEE, 49j 374, TEE assessment 1 Of midesophageal long-axis, 06, 07j 20j 371 , midesophageal short-axis, 1 7, 1 8j 371 transgastric long-axis, 08, 09f assessment before LVAD placement, 394-395 458-459, 459j 460j 461/ grading, 377-378, 377 t TEE assessment, 378 Aortic dissection classifi cati on, 373, 373j 374, 375t, 49 , 492t coronary artery i nvolvement in, 377 etiologies, 374 inti m al tear in, 375, 376j 493-494, 493/ intramural hematoma in, 375-376, 493-494, 494/ magnetic resonance i maging, 374 mortal ity, 374 aortic See Aortic aneurysm atrial septal, , 1j 446j 598 t sinus of Valsalva, 423-424, 425/ Angiosarcoma, 443 Annotation, of ultrasound images, 32 An nuloplasty, 79 See also Mitral valve repair 497, 497J case study, 494j 495/ chest trauma and, 495-496 diagnosis, mortali ty, 373 surgical repair, 373-374 TEE assessment, 374 Aortic arch 84j 4J Aliasing, 8, 50, 50/ Amniotic fl uid embol ism, 373/ 379-380, 379 t, 380/ en dovascular repair, 496-497 378 TEE assessment, 378, 480-48 , 48 1j 495-496, 495/ types, 378 tumors, 443 TEE assessment associated findi ngs, 213 color-flow Doppler, 207-208, 208t, descending aortic flow reversal, 1 , midesophageal long-axis view, 0/ 0/ 2/ pressure half-time and deceleration sl ope, 209, 1j 2f regurgitant volume, regurgitant fraction, and effective regurgitant orifice area, 1 -2 3, 582t, 588 two-di mensional, 207 vena contracta width, 208, l lj 582t I N DEX 630 Aortic root, Aortic stenosis B t B mode, aortic regurgitation and, Ball-in-cage valve, 3, 3t aortic valve replacement for, 4-2 calcific, 99-200, 200/ continuity equation, 68 Doppler measurements, 29, 30/ low-gradient, 204-205 membranous, 98f 20 1/ pathophysiology, 99-200 severity classification, 202-203, 203t, 582t subvalvular/supravalvular path ology, 204, 204/ 24 , 24 1f 249, 249f 593t, 597t Barlow's disease, 78 Basel ine shift, in Doppler i maging, Beck's tri ad, 356 Bernoull i equation in aortic valve assessment, 20 -202 for i ntracardiac pressure measurements, for left heart pressures, l i m itations, TEE assessment 207 contin uity equation method, di mensionless i n dex, 206 principles, 205-206, 206f 582 t 72 72, 72f 73f 70-72, 73f 588 i n prosthetic valve assessment, 248-249 for right heart pressures, 73-74, midesophageal lo ng-axis view, Bicuspid aortic valve, m idesophageal short-axis view, B ilea£let prosthetic valves 97/ 97/ pressure gradients, 20 -205, 202f 203 t, 204/ two-d imension al, 200-20 , 20 1/ 72-73, 73/ 73-74, for peak and mean gradients, associated findi ngs, 28, 28/ 590t Baxter Perimoum scented biologic valve, characteristics, 99, 200f 8-4 9, 9f 8/ 242, 242/ normal Doppler echocardiographic values, paravalvular regurgitation i n , Aortic valve (AV) anatomy, bicuspid, 590-597 t 260/ TEE assessment Doppler, 247-248, 95, 96/ 99, 200f 8-4 9, 9f 8/ epicardial echocardiography, 454-455, 455/ function, 95 quadricuspid, 248f 250 25 1/ two-di mension al , 250, 250/ Biocor stemless biologic valve, 595t Bioeffects, o f ultrasound, Bio£lo stemless biologic valve, 595t three-dimensional, prosthetic, normal Doppler echocardiographic values, 590-594t 200/ regurgitatio n See Aortic regurgitation Biologic prosthetic valves See Prosthetic valves, b iologic replacement See Aortic valve replacement sten osis See Aortic stenosis Bjork-Shiley tilting disk valves, Blood cysts, pericardia!, 443 TEE assessment "Bow-tie" repair (Al fieri stitch), of m itral valve, deep transgastric long-axis view, 08, ll Of 1 1f 99, 99/ m idesophageal long-axis view, 06, 07f 97-1 98, 97f 98/ m idesophageal short-axis view, 05, 06f 95-1 96, 96f 97/ three-dimensional, 3-2 4, 4f 5f 508f 7-5 8, 8/ transgastric long-axis view, 08, 09f 1 1f 98-1 99, 99/ unicuspid, 200/ Aortic valve area, 68, 582t continuity equation method, 205-206, 206f 582 t normal values, 578t Aortic valve replacement See also Prosthetic valves cardioplegia delivery i n , "Bubble study," of patent foramen ovale, c Calcium h omeostasis, impaired, Carcinoid heart disease pathophysiology, 95 TEE assessment, 444 tricuspid dysfunction i n , Cardiac i n dex, Atrial septal defect, Atrial sh unt, 598t See also Aortic 1f 446, 446f 598 t 0-4 1 , 0f J f 2/ 432-433, 432/ Atrioventricular canal defects, 5-4 7, 6f t Atrium See Left atri um; Right atri um Autograft, 590 t 245, 252 2t A-wave velocity, 336 224-225, 23 / 204f 67 440-446 aortic tumors, 443 atrial septal aneurysm, benign tumors, i ncidence, 440 , 1f 446, 446f 598t 440-443, 441f 442f 443/ malignant primary tumors, 443 440 normal structures m i m i ck ing, pericardia! tumors, 443 secondary mal i gnant tumors, heart disease 443-444, 444f See also Carcinoid thrombus See Thrombus vegetations, 446, 446f Cardiac output, 67, 67f 27-1 28, Cardiac resyn chron izati on therapy, Cardiac tamponade 68 Atrial switch operations, ATS bilea£let valves, Attenuation, 2-3 234, 234/ Cardiac catheterization, in aortic stenosis, Cardiac masses, 90 245 versus repair, 4-2 TEE assessment, 254-255, 255/ transcatheter/percutaneous, 245-246, 246f 252-253, 253/ Aortom itral conti nuity, 43 Area ejection fraction (fractional area change) , 29-1 30 Area-length meth od, for LV vol ume, 30-1 Arrhythmias, i n hypertroph i c cardiomyopathy, 325 Arrhyth mogenic right ventricular cardi omyopathy, 340-34 atherosclerosis Atrial septal aneurysm, , 444 pulmonic dysfunction in, m itral regurgitation and outcome of, Atherosclerosis, severity classification, 268 Cannulation, TEE assessment duri ng, 397, 398f 399, 399t, 400f Carbomedics bilea£let valves, 242, 242f 250, 590-5 t, 595t pulmonary autograft, Ani factS See Ultrasound artifacts 80, 84f 4f 40, 40f 394, 394/ restrictive/ infi ltrative cardiomyopathy in, 215 i ntraoperative transesophageal echocardiography i n , l eft ventricular outflow tract obstruction after, 332 242, 590t, 593t, 595t after cardiac surgery, 357-358 399 chest radiography, 358 clinical presentation, 356 i n critical i l l ness, 478 differential diagn osis, 362t electrocardiography, 358 after LVAD placement, 28f 308, 466 530-53 , 532/ I N D EX Cardiac tamponade ( Cont ) : magnetic resonance i magi ng, I Congenital heart disease (CHD) (Cont ) : bicuspid aortic valve, 57f 99, 200f, 9, 9f, 9/ pathophysiology, 356-357 regional, 357-358, 364J classification, 406 coarctation of the aorta, TEE assessment, congen itally corrected transposition of the great arteries, 358 pulsed-wave Doppler, 362, 362 t, 363f, 364/ right atrial col l apse, 359, 360f, 1f right ventricular collapse, 359, 36lf, 362 two-dimensional, 358-359, 359f, 360f, 362t Cardiomyopathy arrhythmogen i c right ventricular, classiflcations, 340-34 See Dilated cardiomyopathy See Hypertrophic cardiomyopathy left ventricular non-compaction, 339-340 peripartum, 47 restrictive See Restrictive/ inftltrative cardiomyopathy Tako-Tsubo, 341 -342 Carpentier classification, m itral incompetence, 49-1 , 49f, 50f, 77-1 78, 78/ Carpentier-Edwards scented biologic valves, 243-244, 243f, 250, 59 t, 595t Cavitation, Central venous pressure, i n ferior ven a cava diameter in, 230 Chamber quantiEcation, 74-75 l eft ventricle, 75-77, 75t, 76f, 77t normal values, 571 t right ventricle, 78, 78f, 78t, 79/ Chest trauma, 495 497 See also Aorta, traumatic disruption Chiari network, 38-39, 39/ Children, TEE complications in, 547, 547t hypenrophic Chordae tendineae abnormalities, , 52f, 53/ 44, 75 arti Ecial, 80 commissural, 75, 76/ leaflet, 76, 76/ anatomy, transposition, for m itral valve repair, Closure backflow, 248 coronary artery anomalies, coronary fistula, 423 423 double-outlet right ven tricle, 430, 43 1/ 223, 223 t, 224, 8, 8/ 406 m itral valve anomal ies, patent ductus arteriosus, 68, 426 427, 427/ patent foramen ovale, 39 40, 40f, 394, 394f, 396-397, 0, 0/ persistent left superior vena cava, 39, 40f, 406 408, 407f, 408/ pulmonic stenosis See Pulmonic stenosis sinus ofValsalva aneurysm, 423 424, 425f subaortic stenosis, 42 422, 42 1f, 422/ supravalvular aortic obstruction, 424 surgical procedures atri al switch operations, 432 433, 432/ 431 432, 432/ Glenn shunt, 430 43 , 43 1/ Rastelli procedure, 433 Ross procedure, 245, 9, 432 TEE assessment, 406 tetralogy of Pallor, 235, 235f, 236f, 420 42 , 420/ transposition of the great arteries, 428 429, 429/ truncus arteriosus, 428 univentricular heart, 427 428 ventricular septal defect, 4 5, 3f, 4f, 5/ visceral situs, 406 Fontan procedure, Congenitally corrected transposition of the great arteries, 429 430, 430/ Conservation of flow, 80, 82-1 83/ 50 Coarctation of the aorta, 380, 424 426, 426/ Color kinesis, 36-1 37, 37/ Color-flow Doppler, 8, Sf, 9/ aliasing, 50, 50f, 1/ in ao rtic dissection, 375, 376/ in aortic regurgitation, 207-208, 208t, 0/ in aortic stenosis, 203 i n m itral regurgitation, 55 in m itral stenosis, 67f for propagation velocity assessment, 283-285, 284/ of prosthetic valves, 247-248, 248/ stented biologic, 250 tilting disk, 249, 249/ for pulmonary venous flow profile, 277 in pulmonic regurgitation, 233/ in pulmonic stenosis, 236 strengths and weaknesses, 66 system controls, 22-25, 24f, 25f, 25t i n tricuspi d regurgitation, 226, 227f, 229f, 30 , 1/ Commissurotomy, 80 Compliance, 270 Compression 28-29, 28/ 9-20, 20/ Congenital heart disease (CH D), 406 433 anom alous pulmonary venous return, 408-1 09, 408f, 409/ atrial situs, atrioventricular canal defects, 7, 6f, t i n two-dimensional i magi ng, 429 430, 430/ i n cidence, 316 i n Doppler imagi ng, 380, 424 26, 426f Ebstein's anomaly of tricuspid valve, dilated Clutter, 63 68, 587 Constrictive pericarditis chest radiograph, 352/ clinical presentation, 352 338-339, 338t, 339f, 362 t electrocardiography, 352 hemodynamics, 352, 353/ magnetic resonance i maging, 353, 353/ pathophysiology, 352 differential diagnosis, T E E assessment M-mode, 354 pulsed-wave Doppler, 354-355, 362t 355-356 two-di mension al, 338, 339f, 353-354, 362 t Continuity equation, 68, 69/ for aortic valve area, 205-206, 206f, 582t for m i tral valve area, 65-1 67, 65f, 67f, 580 t in prosthetic valve assessment, 248 tissue Doppler, Contin uous quality i mprovement, i n perioperative TEE service, 550-5 , 550t Contin uous-wave Doppler, in aortic stenosis, 7f, 202, 202f, 204, 204f in left ventricular outflow tract assessment, 206, 206/ 272, 273/ , 1J in mitral stenosis, 63, 63/ i n pulmonic regurgitation, 235 i n pulmonic stenosis, 236, 236f versus pulsed-wave Doppler, 25, 26/ strengths and weaknesses, 66 system controls, 26-29, 27f, 28f, 29f, l t i n tricusp i d regurgitation, 227-230, 230f, 23 , 231/ in mitral i nflow assessment, in mitral regurgitation, 26f, 632 I N D EX Contractility, 74 Contrast-enhanced TEE for endocardial border detection, 520-521 , 1/ for left ventricular systol ic function assessment, 37-1 38 for perfusion imaging, 522-523, 523/ pulsing i n terval versus video intensity, tech n iques, -522 Contrast-enhanced ultrasonography contrai ndications, 520 contrast agents, 9-520 right ventricular 549 Dilated cardiomyopathy (DCM) clinical presentation, eti ologies, 6, 7t 574/ 423 Crawford classification, aortic aneurysm, 373/ See also Aortic aneurysm Crista term inalis, 36, Critical care, TEE in, Current Procedure Term i n ology (CPT) codes, for TEE, Doppler, Christian, display, 63, 65 for hemodynamic assessment 520 See Hemodynamic assessment high pulse repetition frequency, 66, 66f pulsed-wave See Pulsed-wave Doppler Double-oudet right ventricle, 430, 43 1/ Double-switch operation, 429 Down syndrome, dP/dt, 306, 306t, 307/ Duromedics bil eaflet valve, 595 t Duty factor, D-wave velocity, 276, t Dysphagia, after TEE, 546 E E/A ratio, 1 , 2t Ebstein's anom aly, tricuspid valve, 55 , 5 t, 554 374 See also Aortic dissection Deceleration slope, i n aortic regurgitation, 209, Deceleration time, mitral valve, 65, 27 , 288t Decibels (dB), 63 Doppler effect, Doppler shift, 6-7, 63, 64f, 587 Doppler tissue i maging See Tissue Doppler imaging (TDI) Doppler ultrasound, 6-7 color-flow See Color-flow Doppler contin uous-wave See Contin uous-wave Doppler D 3-dB rule, 20 De-airing, in LAVD placement, 396, 397/ DeBakey classification, aortic dissection, 373f, Distance, I Dobutamine stress echocardiography, in dilated cardiomyopathy, 8-3 37f, 38, 38/ 475-48 aortic injury, 480-48 , 48 1/ cardiac tamponade, 478, 479/ complications, 475-476 diagnoses, 476t diastolic function, 478 embolic source, 480, 480/ endocarditis, 479-480, 480/ hypertrophic cardiomyopathy, 478 hypovolemia and preload, 476-477 hypoxemia, 479, 479/ i ndications for use, 463t, 475, 476t, 477t, 544, 544t i ntracardiac thrombi, 478 left ventricular function, 477 patient preparation, 476 pulmonary embol ism, 478 regional wall motion abnormali ties, 477 right ventricular function , 477-478 versus transthoracic echocardiography, 475 trauma, 480 valvular function, 478 Cross-sectional area (CSA) , 67, 466 Cryolife stendess biologic valve, t Depth gain compensatio n (DGC), Depth settings, 22, 22/ 32 1/ 322-323, 323/ prognostic value, 323 right ventricular diastolic functi on, 322 tricuspid valve l esions, 323 two-dimensional, 8-3 9, 8f, 9f, 320/ ventricular systolic function, 9-320 thrombi in, 9, 320/ tricuspid regurgitation and, 323 Di mension l ess index, 206 Dip and plateau (square-root) sign, 352, 353/ mitral valve lesions, Coronary sinus congenital defects, 1 flow patterns in tricuspid regurgitation, 227, 229/ TEE assessment, 39, 39f, 40f, 1 2-1 3, 1 3/ Coumadin (warfari n) ridge, ! If, 42, 42f, 08 Defin iry contrast agent, Density, I in heart fai lure, 388 See also Heart fail ure i ncidence, 6-3 left ventricular hypertrophy i n , 324, 324/ mitral regurgitation and, 79, 322-323, 323/ pathophysiology, TEE assessment, 7-3 left ventricular diastolic function, 320-322, 523 Coronary artery bypass graft (CABG) m i tral regurgitation before and after, ! 86- 87 wall motion worsen ing fol lowing, 33 Coronary fistula, See Right ventricular diastol ic function Di gital Imaging and Com munication i n Medicine (DICOM) standard, Controls, ultrasound system See Ultrasound system trols CoreValve rranscatheter aortic valve bioprosthesis, 245, 253, 253/ Coronary arteries congenital anomalies, 423 perfusion beds, 02f, 34f, 573f, grading algori thm, 576 t left ventricular See Left ventricular diasrolic function 522, 522/ for myocardial blood flow assessment, for particle image velocimetry, 523-524, 524-525/ principles, 9-250 for sonothrombolysis, 523 for targeted drug and gene del ivery, Diastolic function/ dysfunction age and, 576t classification, 575t ! 1f, 2/ 223, 223 t, 224, 7-4 8, 8/ Ech i nococcus cysts, 443 EchocomTEE simul ator, 569 Edge shadow, 46 Edwards bileaflet valves, t Effective regurgitant orifice area aortic valve, 1 -2 3, 582 t, 588 mitral valve, 5-1 58, 579 t, 588 Ejection fraction left ventricular, 30-1 , 586 right ventricular, 306 Ejection phase indices, 29-1 30 El Khoury classification, aortic regurgitation, 19 Electrical alternans, Electrical noise, 48 358 207, 208f I N D EX Embolism I 633 Fractional area change (area ejection fraction) amn iotic fluid, left ventricle, 471 pulmonary See Pulmonary embolism Emergency care, TEE in, 484-500 29- 30, 586 306 t 29, 586 right venrricle, 306, Fractional shorten ing, aortic dissection Frame rate, cardiac arrest, See Aortic dissection 486-488 case study, 486f 487/ pulseless electrical activity, 488-490, 489f duri ng cardiopulmonary resuscitati on, 490-49 chest trauma, 495 with aortic i njury, 495-497, 495f 497t penetrating, 497 complications, 547-548 hypotension, unexplai ned, 498-500, 498f 500f hypoxia, unexplained, 486t, 500 i ndications for use, 484, 485t, 486t versus transthoracic echocardiography, 484-485 Endocardial border enhancement, 520-52 , 1f Fraunhofer wne, Endocardial cush ion defecrs (atrioventricular canal defects), Freeze control, ulrrasound systems, , 20-2 , 1/ Frequency bandwidth , Fresnel zone, Fundamental frequency, , 1f G Gai n in pulsed-wave Doppler, 26, 27f 6, 8, 9/ in two-di mensional i magi ng, Gh osti ng artifact, 50 G l e n n shunt, 430-43 , 5-4 7, 43 1f 336 Glycogen storage diseases, H 335 Hancock stented biologic valves, Endocarditis 479-480, 480/ m itral regurgitation and, 79 m itral valve, 480f in prosthetic valves, 257-258, 258f 259f TEE-related, 542 vegetations in, 446, 446f Endomyocardial fibrosis, 335-336, 336/ Endovascular aortic repair (EVAR), 379-380, 379t, 380/ Enhancement, 48 Harmonics, See al.ro Left ventricular diastOlic function 388 economic impact, 387 heart transplantation for See Heart transplantation incidence, 387 dilated cardiomyopathy in, mechanical ci rculatory support for i ntra-aortic balloon pumps, 393, left ventricular assist devices i ndications for use, 458 probe preparation, 454 assist devices right ventricular assist devices, 399, 400/ Heart transplantatio n tOmographic views, 458-459, 459f 460f trai ning guidelines, 459-460 surgical techniques, 389 TEE i n d o n o r heart assessment, Epicardial echocardiography probe preparation, 454 387-388, 388t 389-392, 389t, 390t, 39 1f 392/ postOperative period, 392, 392t pretransplant period, 388-389 rej ection i ndicators, 392t Heartworks si mulatOr, 569 Hemochromatosis, 336 i ntraoperative monitoring, 247 tomographic views aortic valve long-axis, 454-455, 455/ 454, 455/ left ventricular basal short-axis, 455, 456f left ventricular long-axis, 457, 457/ left ventricular mid short-axis, 455, 456f right ventricular outflow tract, 457, 458f two-chamber, 457, 457/ trai ning guidel i nes, 459-460 aortic valve short-axis, Esophageal pathology, as contraindication tO TEE, Hemodynamic assessment in constrictive pericarditis, contractility, European Society of Cardiology, classification of aortic dissecrion, 37f 38, 38/ 31 , 2t of Special Competence i n Perioperative Echocardiography) 590t F 43, 44f Fibrin strands, i n prosthetic valves, 259-260 Fibroelastic deficiency, 78 Fibroelasroma, 442, 442/ Fibroma, 442 Focal point, of ultrasound beam, 4, 4f Focal zone, 22 Fontan procedure, 43 -432, 432f 68 67, 67f i ntracardiac shunt, 68 pressure, 70-74, 72f 73f resistance, 74 velocity acceleration, 69-70 flow measurement, 375 t E-wave velocity, Examination of Special Competence in Perioperative Echocardiography See PTeXAM (Exam i nation 352, 353f 74 flow conservation, 545 Eustachian valve, Fabry disease, 336 False tendons, left ven tricle, 393f See Left ventricular (LVADs) surgical decision making a n d , 460-46 Extended Biocor stemless biologic valve, , 1/ -22, 1/ Heart fail ure diastolic, 266 Epiaortic ultrasonography (PTeXAM) 243, 243/ 250, t, 596 t Harmonic frequencies, in critical i l l ness, prosthetic valves, 29-30 Frequency, 6f 6t Endocardial fibroelasrosis, Hemodynamic disturbances in critical i l lness, 475, 476f 462, 463 t in non cardiac surgery, Hemodynamic mon itOri ng, with TEE, 466 cardiac output measurement, 466 i ntracardiac pressure measurement, 468, 468t 466-467, 467/ preload recruitable stroke volume, 467 versus pulmonary artery catheter, 466 l eft ventricular preload measurement, Hepatic venous flow patterns in dilated cardiomyopathy, 322 in right ventricular function assessment, 286, 289f 303, 303f 2t, 322 in tricusp id regurgitation, 226-227, 229f I N D EX 634 Hibernati ng myocardium, 318 High pulse repetition frequency (HPRF) Doppler, Hodgki n's lymphoma, 444 Homograft prosthetic valves, Huygens pri nciple, 66, 66f Jatene procedure, K 245, 252, 592t Kussmaul's sign, Hypereosinop h i l i c syndrome (Loffler endocarditis), Hypertroph ic cardiomyopathy (HClvf) 592t, 596t 592 t Lambl's excrescences, 43-44, 44j 442, 442/ Lateral gain compensation (LGC) , Lateral resolution artifact, 46 Leaflet extension, for mitral valve repair, 80-1 , 85/ Labcor Synergy stented biologic valve, 324-325 i n critical i l lness, 478 eti ologies, t, 323 genetic factors, 323 i ncidence, 6, 323 m itral valve repair/replacement in, 352 Labcor Santiago stented biologic valves, 269 clinical presentation, signs, and symptoms, 429 L 335-336, 336/ Hypertension, diastolic heart fail ure and, mortality, J Left atrial appendage anatomic variants, 330, 332 324 43, 43f TEE assessment pathophysiology, three-dimensional, TEE assessment, two-dimensional, 323-324 325 diastolic function, 325 thrombi i n , left ventricular outflow tract obstruction, 324, 328-330, 328j 329f 8j 42-43, 42j 08 395, 396/ Left atri urn (LA) anatomic variants, m itral regurgitation, 328-332, 328/ systolic anterior motion of m itral valve leaflets, 327, 328j 329, 329j 330/ congenital anomal ies, systolic outflow obstruction, development, ventricular function and di mensions, 327, 327/ morphology, 325, 326/ 410 36 571 t epicardial echocardiography, Hypertrophy left ventricular, 324, 324/ See also Dilated cardiomyopathy right ventricular, 304, 304f Hypoten sion, unexplai ned, cardiac etiol ogi es, case study, 36 left atrial appendage, 42-43, 42j 43f l igament of Marshall, 42, 42/ quantification methods, 486t 498-499 78 TEE assessment after heart transplantation, 498/ hypovolemia as cause of, 390, 392/ 08, 1 1j 1 2/ 73-74, 468, 468 t, 589 tomographic views, 499 pulmonary embolism as cause of, Hypovolemia after LVAD placement, hypotension i n , 457, 457/ m itral valve and, myxoma, 440-44 , 44 1f 498j 499-500, 500f Left heart pressures, Left ventricle (LV) anatomic variants 399 499 false tendons, measurement, 43, 44/ 43-44, 44f left ventricular bands, 44, 44f nodule of Arantius, 44 apical thrombus, 9, 320/ congenital ano mal ies, contractility, 32-1 33, 32/ coronary blood supply, 99, 02/ diasrolic function See Left ventricular diastolic function TEE assessm ent in l iver transplantation, di mensions and geometry left ventricular volumes i n , 462 TEE assessment, 462, 476-477, 488, 499 ICD-9 diagnostic codes, Inferior vena cava di mensions, 52-5 54t 57 t 308, 1/ 47 , 47 1/ 11 -1 2, 11 2/ Inftltrative cardiomyopathy See Resttictive/inftltrative cardiomyopathy tomographic views, (RICM) Inflow can nula, TEE assessment in LVAD placement, 397, 398j in RVAD placement, Intact stented prosthetic valve, Interatrial septal aneurysm, 399, 399t, 400f 592t 39 , 1j 443, 443/ tomographic views, 08, 11 0-11 , 1 2/ Intra-aortic balloon pumps (IABPs), 393, 393/ Intracard i ac pressure measurement, 72-74, 73j 468, 468t, 588 Intracardiac shunts, 68 Intramural hematoma, 375-376 See also Aortic dissection Ionescu-Sh iley stented biologic valve, 592t, 596t Ischemic heart disease, m itral regurgitation i n , 78-1 89, 86 Isovolumic relaxation period (IVRT) , 270, 272t, 273j 28 t lipomatous hypertrophy, 26-1 27 75-77, 75t, 76j segmentation and nomenclature, 99j 34, 34j 573/ 455-457, 456j 457/ m itral valve and, 44, 54, 54/ morphological features, t myxoma, 44 outflow tract See Left ventricular outflow tract (LVOT) outflow tract obstruction See Left ventricular outflow tract epicardial echoca r diography, , 1j 446, 446j 598t Interatrial septum after heart transplantation, mass, quantification methods and calculations, 26-1 27, 586-587 reference values, 77t, 571 t 399 Intensity, I Lambl's excrescences, obstruction (LVOTO) systolic function See Left ventricular systolic function TEE assessm ent after heart transplantation, 390, 390t , 93/ m idesophageal lo ng-axis view, 93, 95/ midesophageal two-chamber view, 93, 94/ m i rror image artifact, 48f three-dimensional, 38, 38j 1 j 3-5 5, 7, 7/ transgastric ap ical short-axis view, 94, 98j 99 transgastric basal short-axis view, 94, 96f m idesophageal four-chamber view, I N D EX Left ventricle (LV), TEE assessment ( Cont.): 94, 97f transgastric two-chamber view, 99, 1/ wall motion analysis, 99 wall th ickness, 26 transgastric mid short-axis view, Left ventricular assist devices (LVADs), TEE assessment postoperative period, 399, 399 t pre-procedure aortic pathology, 394-395 aortic valve insuffi c iency, 395 left hearr thrombus, 395, 396/ m itral stenosis, Left ventricular systolic function, TEE assessment patent foramen ovale, 394, 394/ 396-397 separation fro m cardiopul monary bypass Liver transplantation, TEE i n , 335-336, 336/ Longitudinal resolution, anesthesia i nduction, left ventricle, postoperative care, Lysosome storage diseases, 320 grading, 285, 286[, 287f, 288[, 288 t, 289f, 575t i n hypertrophic cardiomyopathy, 325 measurements, 269-270 m itral regurgitati o n and, 322 pathophysiology, 268-269, 269/ phases, 266-268, 267f TEE assessment, 270 after heart transplantation, 390, 390 t m itral an nulus tissue Doppler imaging, 280-282, 28 -282/ m itral inflow See Mitral inflow normal values, 272 t perioperative, 287, 289 propagation velocity, 283-285, 284f pulmonary venous flow See Pul monary venous flow strain and strain rate measurements, 282-283 Left ventricular ejection fraction (LVEF) , 30- , 586 Left ventricular non -compaction cardiomyopathy, 339-340 M M mode, i n ao rtic regurgitation, 209, in aortic stenosis, 205-206, 1[, 2/ 206f epicardial echocardiography, 45 5f TEE assessment, 67, 67[, 68[, 04-1 06, 07/ Left ventricular ourflow tract obStruction (LVOTO) 332, 333/ 87-1 88, 88-1 89[, 90, 260, 332, 333/ 324, 325, 326[, 327-33 , 328[, 329/ Mal ignant lymphoma, Malignant melanoma, 444 443-444 Marfan 's disease m itral regurgitation i n , 78 pulmonic regurgitation i n , 223 t tricuspid regurgitation i n , 223, 223t, Master synchro n izer, Matrix array, cardiac output, 27-1 29, 28/ color kinesis for, 36-1 37, 37/ ejection phase i ndices, 29-1 30 in hypertrophic cardiomyopathy, 325 isovolurnetric indices, 32-1 33, 32/ load dependence and i ndependence, 25-1 26, 27 t pressure-volume relations, 25, 26/ quantitative approaches, 30-13 , / regional, 33-1 34 TEE assessment 7-1 38 Doppler tissue i magin g, 34- 35, 35/ speckle tracking i maging, 5, 36[, 37f 227f 5t MCRI On-X bileaflet valve, Mean pressure gradients, 592t 72, 72/ Measurements, i n ultrasound images, 30-32 Mechanical circulatory support intra-aortic balloon pum ps, 393, left ventricular assist devices 393f See Left ventricular assist devices (LVA Ds) right ventricular assist devices, Mechanical i ndex (MI) , 399, 400/ 9, 20 See Prosthetic valves, mechan i cal Medtronic Advantage bileaflet valve, 592 t Medtronic Freestyle scentless biologic valve, 244, 244f, 592t 596 t Medtronic Mosaic stented biologic valve, 593t Medtronic-Hall tilr i n g disc valves, 24 -242, 24 1[, 248, 249, 249f, 592t Meridional wall stress, 586 Mesothelioma, pericardia!, 443 MetaStases, cardiac, 443 Micro bubbles See Contrast-enhanced TEE; Contrast-enhanced Medtronic Intact Porcine stented biologic valve, ultrasonography Left ventricular systolic function contrast-enhanced, 336 Mechanical prosthetic valves Left ventricular ourflow tract (LVOT) in hypertrophic cardiomyopathy, 468-469, 469f 469-470, 469/ vascular anastomosis assessment, clinical i mportance, 266 i n dilated cardiomyopathy, after m itral valve repair/replacement, 46 468 470 pulmonary artery clam p i ng, Left ventricular diastolic function after cardiac procedures, 470-47 , 47 1/ Loffler endocarditis (hypereosi noph i l i c syndrome), i nflow cannula, 397, 398/ 398 ourflow cannula, 397-398, 398/ patent foramen ovale, 396-397 right ventricular dysfu nction, 397 , 1[, 443, 443/ 443 Longitud i n al resolution artifact, Lung transplantation, TEE i n aortic valve, 397 de-airing, 396, 397f ( Cont.): 135-1 36, 35/ three-dimensional, 38, 38/ torsion/twist, 37, 37/ wall stress, 32 Leukem ic myocardial infi ltration, 444 Ligament of Marshall, 42, 42/ Lillehei -Kaster tilting disc valve, 596t Linear switched arrays, 3, 5t Lipoma, 442 Lipomatous hypertrophy, i nteratrial septum, right ventricular dysfunction, tricuspid regurgitation, 395 635 strain rate i magi ng, Liposarcoma, 395 I Midesophageal views, 92[, 572/ aorta long-axis, short-axis, aortic valve long-axis, 06, 07[, 20/ 1 7, 1 8/ 06, 07[, 96[, 97-1 98, 97[, 0[, 572t 05, 06[, 95-1 96, 96/ l eft atrial appendage, 08 left atrium, 1 , 1 2/ l eft ventricle, , 93 four-chamber, 93/ long-axis, 95/ two-chamber, 94f short-axis, 636 I N D EX Midesophageal views ( Cont.) : m itral valve, 03[ atrial perspective, 04[ four-chamber, 00, 45-1 46, Mitral stenosis ( Cont.) : measurement, 69-70, pathophysiology, TEE assessment 45f, 46[ long-axis, 95f, 02, 45f, 46, 47[ m itral com m issural, 05f, 45f, 46, 46[ two-chamber, 94f, 1 , 45f, 46, 46[ pulmonary valve, 1 4, 11 7, 1 7[ right atrium, 1 2-1 3, 1 2[ right ventricle bicaval, -302, 1f four-chamber, 1 3-1 4, m itral valve area by continuity equation, m itral valve area b y deceleration time, m itral valve area by pressure half time, 233[ 575t, 576 t 27 1f, 272f, 272 t, TEE assessment 362t, 363[ in left ventricle diastolic dysfunction , 320-32 , l i m itations, 276 methods, 271f, 273f, 274f, 275t i n restrictive left ventricular fi l l i ng, 337, 337[ techn ical recommendations, 27 -273 Mitral regurgitation after cardiac surgical procedures, 86-1 87, after heart transplantation, 392 1f, 321 t 90, 332, 333[ i n dilated cardiomyopathy, 79, 322-323, 323[ eti ol ogies annul us abnormali ties, chordae tendineae abnormalities, , 52f, 53[ degenerative disease, 78 dilated cardiomyopathy, 79, endocarditis, 79 327-329, 328f, 329[ chordae tendineae, 44, 75-1 76, 76[ leaflets and com m l ssures, 43, 44f, 77, papi llary m uscles, 44 congenital anomalies, endocarditis, 480[ left ventricular abnormalities, 54 papillary m uscle abnormalities, , 54 rheumatic disease, , 1f, 79 functional classification, 49-1 , 49f, 50f, left ventricular diastolic function and, 77-1 78, 78[ 322 measurement, 68, 69-70, 1f with papillary muscle rupture, 490, 490[ with prosthetic valve, 247, 247f, 248f severity classification, 56t, 578t, 579t TEE assessment color-flow Doppler, 55 contin uous-wave Doppler, 26f, , 1[ proximal isovelocity surface area, 7lf, 58-1 59, 58f, 59f, 60[ pulmonary venous flow patterns, 60, 60[ pulsed-wave Doppler, 26f, 60, 60[ regurgitant volume, regurgitant fraction, and effective regurgitant ori fice area, 55-1 58, 579 t, 588 two-di mensional, 54 55 vena contracta, 47f, 5, 57[ Mitral stenosis aortic regurgitation and, 3, 3t classification, 62t, 579t, 580t congen ital, 62 77[ 455, 456f, 457[ prosthetic no rmal Doppler echocardiographlc values, 595-597 t three-dimensional echocardiography, 1 , 3f regurgitation See Mitral regurgitation repair See Mitral valve repair replacement, 240, 253-254 See also Prosthetic valves sten osis See Mitral stenosis systolic anterior motion, 327-33 , 328f, 329f, 330[ TEE assessment, 00-1 04, color Doppler i magi ng, 148 m i desophageal four-chamber view, 00, 45-1 46, 45f, 46[ m i desophageal lo ng-axis view, 95f, 02, 45f, 46, 47[ m i desophageal m itral com m i ssural view, 05f, 45f, 46, 46[ midesophageal two-chamber view, 94f, 1 , 45f, 46, 46[ three-dimensional, 32, 48-1 49, 1 for annulus and leaflet geometry model i n g, for an nulus animation, 47f quantitative, 3, repaired, 4[ 6[ xPlane mode, 507f zoom , 508[ tissue Doppler imaging, 280 83, 28 -282[ transgastric basal short-axis view, 96f, 02, 47-1 48, 48[ transgastric two-chamber view, 04, 47, 47f, 48[ Mitral valve area, 68 by conti nuity equation, 65-1 67, b y deceleration time, 65, 580t determ ination methods, 580 t normal values, 578 t by pressure half time method, Mitral valve prolapse, Mitral valve repair 65f, 67f, 580t 64 65, 580t, 587 49 i n annular calcification, complications, 90 durability, 87 i n hypertrophic cardiomyopathy, i ndicati ons, 83 330, 332 left ventricular outflow tract obstruction after, 395 33f attial perspective, 32f, 04f, 46[ duri ng diastole, 44[ full volume, 0f, 5f m idesophageal view, 03f, 47[ prosthetic, 1 , 3[ ischem ic disease, 78-1 79, 86 leaflet abnormali ties, , 1[ etiologies, 62 LVAD placement and, Mitral valve ( MV) anatomy, 00, 03-1 04[ annulus, 43 44, 75 epicardial echocardiography, 288t, 575 t, 576t, 577[ i n cardiac tamponade, 65, 580 t 64 65, 580t m itral valve resistance, 67-1 68 pressure gradient, 64, 64f, 580t three-dimensional i maging, 68, 68[ two-di mensional imaging, 62 64, 63f thrombi and, , 1f, 63[ Mitral valve replacement, 240, 253-254 See also Prosthetic valves 298-299, 299[ in conmictive pericarditis, 355, 355[ normal patterns and basic variables, 270 , 65-1 67, 65f, 67f, 580t i nflow-outflow, 1 4, 1 5f, 300, 300f, 30 1[ tricuspid valve bicaval, 1 3f, 1 four-chamber, 222, 224[ right ventricular inflow-outfl ow, 1 4, 222, 225f, 232, s hort-axis, 232, 233[ Mi rror im age artifact, 48, 48[ Mitral inflow (transmitral Doppler flow) abnormal patterns, 273-275, 275f, 288t, 70f, 1f 332, 333[ 87-1 88, 90, I N D EX Mitral valve repair ( Cont.): 39-40, 40j 394, 394j 396-397, 0, 0/ 257 27 , 288 t Patient-prosthesis m ismatch (PPM), success rate and surgical tech niques Peak A velocity, Peak dP/dT See dP/dt 256, 257f operative risk, 87 annuloplasty, Peak E velocity, 79 "bow-tie" repair (Al fieri stitch), conunissurotomy, 80, 84/ 80, 82- 83/ 80 leaflet extension, 80-1 , 85/ leaflet resection, 79- 80, 79J papillary m uscle shortening, 80 patch closure of leaflet perforation, 80, 83/ 181 sliding leaflet tech n ique, 80, 1(, 90 Mitral valve replacement, 240, 253-254 See also Prosthetic valves Mirroflow stented biologic valve, 593 t, 596t Moderator band, right ventricle, 43, 43J Monitori ng, with TEE, 463-468 hemodynam ic, 466 cardiac output measurement, 466 i ntracardiac pressure measurement, 468, 468 t left ventricular preload measurement, 466-467, 467/ preload recruitable stroke vol ume, 467 versus pulmo nary artery catheter, 466 myocard i al ischemia, 464-466 Mustard procedure, 429 Myocardial contrast echocardiography, resection of secondary chordae tendi neae, speckle tracking echocardiography, 283, 527-533, 528-53 1] 532/ strain and strai n rate curves, 35-1 36, 35j 524-526, 526J 526-527, 526/ Myocardial ischemia echocardiographic man i festations, 33 464-466 Myocardi.al performance i ndex (MPI), Myxoma, Pericardium anatomy and physiology, tumors, 443 Period, 351 Perioperative TEE, 540-554 billing a n d reimbursement, Myocardial deformation imagi ng tissue Doppler strain, 271 , 288t 72, 72/ Pectinate muscles, , 42/ Pentalogy of Fallot, 420 Perfusion i magi ng, , 522-523, 523/ Pericardia! effusion See also Cardiac tamponade in aortic dissecti on, 377 in critical i l l ness, 478, 479/ magnetic resonance i magi ng, 57f pathophysiology, 356 versus pleural effusion, 488, 490/ severity classification, 598t T E E assessment, 44-45, 44j 358-359, 488 acute versus chronic, 479/ m idesophageal four-chamber v iew, 489f midesophageal lo ng-axis view, 360j 478 midpapil lary short-axis view, 359/ transgastric short-axis view, 489f Pericarditis, 35 -352 See also Constrictive pericarditis Peak gradient, 80 chordae transposition, TEE monitori ng, 306-307, 306 t, 308j 587 440-44 , 44 1/ N National Board of Echocardiography (NBE), 560-5 5 , 5 t, 552-554t, 554 542, 545-548, 546t, 547t continuous quality improvement, 550-5 , 550t contrai ndications, 545 database management, 549 equipment and probe maintenance, 540-541 image acquisition, storage, a n d retrieval, 548-549 i ndications for use, 543-545, 544t organizational logistics, patient preparation, 541 -542 probe insertion, 87, 542-543 probe man i pulation, 87-89, 89j 90f reports, 549-5 50, 549 t, 50 t complications and safety, trai ning and certification Near field clutter, 48 Nodule of Arantius, 44 Nyquist l i m it, accreditation of adult cardiothoracic fellowsh ips, advanced level objectives and requirements, in Austral ia and New Zealand, 564 basic level objectives and requirements, Obesity, as TEE risk factor, Oblique sinus, 548 45, 45j 35 562 560 t, 561 -562 559t, 563, 569-570, 569t in Europe, 563 guideli n es, 561 Omn icarbon tilting disc valve, National Board of Echocardiography (NBE), O m n iscience tilting disk valve, objectives, 593t, 596t 242, 593 t On-X bileaflet valve, 242, 250, 25 1j 597t Optison contrast agent, 9-520 Ostium primum defects, 0-4 1 , 2/ Ostium secundum defects, 0, 1 / recertification, 562, 566 Peripartum cardiomyopathy, 471 Outflow can nula, TEE assessment Persistent l e ft superior vena cava, in LVAD placement, in 397-398, 398j 399 RVAD placement, 399, 400/ p PTeXAM 558, 559t, 560 t See PTeXAM (Exam i nation 442, 442f Papillary muscles i n aortic dissection, 377, 377/ in critical i l l ness, 479, 479/ abnormalities, versus pericardia! effusion, TEE assessment, shorteni ng, for m itral valve repair, Particle image velocimetry, 523-524, Patent ductus arteriosus, 80 524-525J 68, 426-427, 427J of Special Competence in 39, 40j 406-408, 407j 408/ Phased arrays, 3, t Piezoelectric effect, anatomy, , 54 44, 76-1 77, 77/ anterior displacement, 329, 3 1/ rupture, 490, 490/ 560-561 Perioperative Echocardiography) Pleural effusion Papillary fibroelastoma, 637 Patent foramen ovale, prosthetic mi tral ring i n , artificial chordae, I Pompe disease, Power, 45, 46/ 336 , 20 Pregnancy, TEE in, Preload, 26, Pressure, 47 466-467 488, 490/ I N D EX 638 Pul monary arrery(ies) Pressure gradients in aortic stenosis, 20 -204, 203t, 204[ i n tricuspi d regurgitation, 227-230 th rombus i n , tomographic views, 1 7, 1 8[ 466 245 Pul monary artery catheter, Pressure half-time in aortic regurgitation, Pul monary autograft, for m itral valve area, Pulmonary embolism 209, 1f, 2[ 64- 65, 587 in pulmonic regurgitation, 235 i n tricuspi d stenosis, 23 , 232t Pri ma prosthetic aortic valve, 593t Probe, transesophageal i nsertion, ( Cont.): 464[ after LVAD placement, 399 hypotension and, 498f, 499-500 TEE assessment, 462-463, 464f, 465t, 498f, 499-500, 500[ 74 08, 1 1[ Pulmonary vascular resistance (PVR), Pul monary vei n (s), 87 manipulation, 87-89, 89f, 90f Propagation speed, Propagation velocity, 283-285, 284f, 288t Pulmonary venous (PV) flow abnormal patterns, 28t, 278, 279f, 575 t 276-277, 277f, 288t, 575t, 576 t, 577[ normal patterns and basic variables, Prosthetic valves biologic TEE assessm ent homografts and aurografts, 24 stented, 243-244, 243f, 250, 252f, 590-597t stendess, 244, 244f, 252, 253f, 590-597t complications 320-32 , 32 1f, 32 t 337, 337[ resrriccive/inftl tracive cardiomyopathy, 362 t in Pulmonic regurgitation obstruction secondary to tissue adhesives o r glues, paravalvular regurgitation, 260, 260f 257 patient-prosthesis m ismatch, thrombosis and hemorrhage, 258-259, 260[ 247 epicardial echocard iographic assessment, 24 mechanical 24 , 24 1f, 249, 249f, 593t, 597t bileaflet See Bileaflet prosthetic valves tilting disk, 24 -242, 24 1[ 256 256 590-594t 595-597t TEE assessment in aortic posi tion, Doppler eval uati on, 234-235, 234 t 234, 234f, 234 t etiologies, 223t, 235, 235[ 419 severity assessment, 583t TEE assessment, Doppler evaluation, 236, 236f, 236t two-di mensional, 235, 236t i ncidence, Pulmonic valve 224f, 232 300 t, 578 t regurgitatio n See Pulmonic regurgitation sten osis See Pulmonic stenosis reference values, normal Doppler echocardiographic values m itral valves, TEE assessment anatomy, m itral rings, aortic valves, 223 t, 233-234 234 t, 583t two-di mensional, Pulmonic stenosis primary failure, 260 thromboembolism, 259 bal l-in -cage, etiologies, severity assessment, 260-261 challenges, Doppler evaluation, in left ventricular diastolic dysfunction, 257-258, 258[ fibrin Strands, 259-260 LVOT obstruction, 260 multiple, 362 t 362 t 277-278, 278[ in conStrictive pericarditis, i n restrictive left ventricular fi l l i ng, en docarditis, i n d ications, in cardiac tamponade, TEE assessment 254-255, 255[ deep transgastric right ventricular outflow view, 233 m idesophageal right ventricular i nflow-outflow view, Doppler evaluati on, m idesophageal short-axis view, homografts and autografts, three-dimensional, 247-249 252 in m itral position, 253-254 percutaneous aortic valve, 252-253, 253[ in pulmonic position, 256 three-dimensional, 247, 1f, 252[ in tricuspi d posicion, 255-256 Proxi mal isovelocity surface area (PISA), 69-70 for m itral regurgitation, 1f, 58-1 59, 58f, 59f, 60f, 580t fo r m itral stenosis, ?Of, 1[ for tricuspi d regurgitation, 226, 228[ Pseudo truncus, 28 PTeXAM (Exam i n ation of Special Competence i n Perioperative Echocardiography) application process, 565-566 566, 567-568t, 568-569, 569t 558-560, 565 content and preparation, development, format, results, diastolic pressure, transgastric right ventricular i n flow-outflow view, upper esophageal short-axis view, Pulmonic valve area, 583 t Pulmonic valve replacement, Pulse duration, 2, 2f 256 Pulse repetition frequency (PRF) , Pulse repetition period, Pulsed ultrasound, 2, 65, 65[ 2, 2f Pulsed-wave Doppler, aliasing, 232 1 7, 1 9f, 232, 233[ 7-8, 7[ 50, 50[ for aortic regurgitation assessment, 1 , 2[ in cardiac tamponade, 362, 362t, 363f, 364[ in constrictive pericarditis, 354-355, 362t 25, 26[ for hemodynamic assessment See Hemodynamic versus continuous-wave Doppler, of hepatic vei n flow, 303, 303[ for m itral inflow assessment, 270, 468-469 468t, 589 78t, t systolic pressure, 308, 0f, 468, 468t, 589 di mensions, 232, 233[ 8-5 assessment 566 566, 569t Pulmonary arrery(ies) clampi ng, in lung transplantation, 1 4, 1 7f, 232, 233[ 246 27 , 275[ 26f, 60, 60[ flow patterns, 60, 60f, 277-278, for m i tral regurgitation assessment, of pulmonary venous 278f, 279f in resrriccive/i n futracive cardiomyopathy, 362 t I N D EX Pulsed-wave Doppler ( Cont.): strengths and weaknesses, 65-66, 65f system controls, 26-29, 27j 28j 29j 30j t time-gating, 66 Pulseless electrical activity, TEE in, 488-490, 489f Pulser, Pulsus paradoxus, 357 Q Quality improvement, in perioperative TEE service, 50-55 , 550t R Radiation therapy, restrictive/inftltrative cardiomyopathy and, 336 Range ambiguity, Range discrimination, Range equation, Rastelli classification, atrioventricular canal defects, 6, 6t Rastelli procedure, 433 Receiver, Reflection, Refraction, 3, 3/ Refraction artifact, 48, 48/ Regional wall motion abnormalities See Wall motion abnormalities Regurgitant fraction in aortic regurgitation, 1 -2 3, 582t in mitral regurgitation, 55-1 58, 579t Regurgitant volume aortic valve, 1 -2 3, 582t, 588 mitral valve, 5-1 58, 579 t, 588 Reject, in Doppler imaging, 29, 29/ Renal cell carcinoma, metastatic, 444, 444/ Renal perfusion imaging, 522-523, 523/ Renin-angiotensin system, 269 Resolution, 5, 6j 46, 46f Restrictive/inftltrative cardiomyopathy (RICM) differential diagnosis, 337-339, 338t, 362 t etiologies, 7t, 333, 334t amyloidosis, 334-335, 335/ endocardial fibroelastosis, 335 hemochromatosis, 336 hypereosinophilic syndrome, 335-336, 336/ idiopathic, 335 sarcoidosis, 336 incidence, t pathophysiology, 333 TEE assessment Doppler evaluation, 336-337, 337j 362t two-di mensional, 333-336, 335j 362t Retroflexion, of probe, 88, 89f Reverberation artifact, 47-48, 47j 48f Reverse piezoelectric effect, Rhabdomyoma, 44 Rhabdomyosarcoma, 443 Rheumatic disease mitral valve disease and, , j 79, 580t tricuspid valve disease and, 223, 224 t Right atrial appendage, -42 Right atrial collapse, 359, 360j 36 1/ Right atrial pressure measurement, 308-309, 1/ in tricuspid regurgitation, 227-229, 230/ Right atrium (RA) anatomic variants, 36, 37f Chiari network, 38-39, 39/ crista terminalis, 36, 37j 38, 38/ eustachian valve, 37j 38, 38/ interatrial septal aneurysm, , 1/ l ipomatous hypenrophy of the interatrial septum, , 1f I Right atrium (RA), anatomic variants ( Cont.): patent foramen ovale, 39-40, 40f pectinate muscles, , 42/ persistent left superior vena cava, 39, 40f right atrial appendage, -42 thebesian valve, 37j 38, 38/ trabeculations, congenital anomalies, development, 36 dimensions, 300t, 571 t myxoma, 44 quantification methods, 78-79 TEE assessment after heart transplantation, 390, 39 1/ midesophageal bicaval view, 1 2-1 3, 1 2j 30 , 1/ midesophageal four-chamber view, 299, 299/ midesophageal inflow-outflow view, 300, 300/ Right heart pressures, 73, 468, 468t Right ventricle (RV) anatomic variants, 43, 43/ anatomy, 298 congenital anomalies, diastolic function See Right ventricular diastolic function dilatation, 304-305, 305j 464/ double-outlet, 430, 43 1/ hyperrroph� 304, 304f LVAD placement and dysfu n ction of, 395-396, 397 mechanical adaptations, 303-305, 304j 305/ morphological features, 0t myxoma, 44 outflow tract See Right ventricular outflow tract (RVOT) quantification methods, 78, 78j 79j 587 reference values, 78t, 300 t, 571 t systolic function See Right ventricular systolic function TEE assessment, 298 after heart transplantation, 390, 39 1/ hepatic vein flow, 303, 303/ midesophageal bicaval view, 30 -302, 1/ midesophageal four-chamber view, 1 3, 298-299, 299/ midesophageal inflow-outflow view, 1 4, 1 5j 300, 300j 30 1f transgastric deep view, 302-303, 303/ transgastric inflow view, 1 4, 1 6j 301 -302, 302/ transgastric outflow view, 302, 303f transgastric short-axis view, 30 , 302/ Right ventricular assist devices (RVADs), 399, 400f Right ventricular collapse, 359, 36 1j 362 Right ventricular diastolic function, 286, 309-3 after heart transplantation, 390 in dilated cardiomyopathy, 322 hepatic vein flow and, 286-287, 289j 1 , 2t, 322 tricuspid annular tissue Doppler analysis, 1 , 2t tricuspid inflow velocities, 0-3 1 , 1j 2t, 322 Right ventricular outflow tract (RVOT) epicardial echocardiography, 457, 458/ measurement, 308 reference values, 78t, 300 t, 571 t Right ventricular systolic function cardiac output, 308, 309f dP/dT, 306, 306t, 307f ejection fraction, 306, 306t fractional area change, 306, 306t myocardial performance index, 306-307, 308/ pulmonary artery systolic pressure, 308, 0/ regional, 305 right atrial pressure, 308, 1f tricuspid annular plane systolic excursion, 306, 306t, 307f velocity-time integral, 308, 309f 639 640 I N D EX Right ventricular systolic pressure, 588 Ross procedure, 245, 9, 432 s Sample volume, Sapien transcatheter aortic valve bioprosthesis, 245, 245/ Sarcoidosis, 336 Scatter reflectors, Scattering, Sector size, 22, 23/ Senning procedure, 429 Seventeen-segment model, left ventricle, 99f, 34, 34f, 573/ Shadowing, 46, 57/ Shone complex, 8, 424 Side lobes, 48-49, 49f Simpson's rule method, for LV volume, 30, 1f, 586 Sinus horns, left and right, 36, 37/ Sinus ofValsalva aneurysm, 423-424, 425/ Sinus venosus, 36, 37f, 1 , 1f, 2/ Situs inversus, 406, Situs solitus, 406, Slicling leaflet technique, for mitral valve repair, 80, 1/ Smoothing, in color-flow Doppler, 24-25 Snell's law, Sonothrombolysis, 523 Sorin Allcarbon tilting disc valve, 597 t Sorin Bicarbon bileaflet valves, 593t, 597 t Sorin Pericarbon stemless biologic valve, 593t Spatial pulse length, 2, 2f Spatial resolution, 5, 6f Speckle tracking echocardiography for cardiac resynchronization therapy guidance, -532, 532/ for myocardial strain and strain rate measurement, 527-533, 528-5 1/ for ventricular function assessment, 35, 36f, 37f, 283 Specular reflectors, Speed errors, 49 Square-root sign, 352, 353/ St Jude Epic stented biologic valve, 243, 243/ St Jude Medical bileaflet valves characteristics, 242, 242f, 593-594t, 597t dehiscence, 259/ TEE assessment, 248f, 250 St Jude Medical stemless biologic valve, 594t Stanford classification, aortic dissection, 373f, 374 See also Aortic dissection Starr-Edwards ball- i n-cage valve, 24 , 24 1f, 249, 249f, 593t, 597t Stented biologic valves normal Doppler echocarcliographic values, 590-597t TEE assessment, 243-244, 243f, 250, 252/ Stemless biologic valves normal Doppler echocarcliographic values, 590-597 t TEE assessment, 244, 244f, 252, 253/ Stitch artifact, in 3D imaging, , 1f Strain, 35, 282-283, 524-526, 526f, 586 Strain rate curve, 525-526, 526/ Strai n rate imaging, 35-1 36, 35f, 283 See also Myocarclial deformation imaging Stroke volume, 67, 68f, 27, 466, 587 Stroke work, 32 Stunned myocarclium, Subaortic stenosis, 42 -422, 42 1f, 422/ S-wave velocity, 276, 2t Sweep speed, 26, 27/ Systemic vascular resistance (SVT), 74 Systolic function/dysfunction left ventricular See Left ventricular systolic function right ventricular See Right ventricular systolic function T Tako-Tsubo cardiomyopathy, 34 -342 Temporal resolution, 6, 6f Teratoma, pericarclial, 443 Tetralogy of Fallot, 235, 235f, 236f, 420-42 , 420/ Thebesian valve, 37f, 38, 38/ Thebesian veins, 423 Thermal bioeffects, of ultrasound, Thermal index (TI), 20 Thoracic aorta, 370-371 , 37 1/ See also Aorta Three-dimensional TEE aorta, 1/ aortic valve, 4, 4f, 5f, 508f, 7-5 8, 8/ artifacts, , f history, 506 imaging technology, 506-5 1 , 507/ 3D color full volume, 509, 1 f 3D zoom, 508, 508/ full volume, 508-509, 509f, 0f, 1 f, 2/ l ive 3D, 508, 508/ transducer, 507f left atrial appendage, 8f, left ventricle, 38, 38f, 3-5 5, 7, 7/ limitations, mitral valve, 32, 48-1 49, 1 for an nulus and leaflet geometry modeling, 33/ for an nulus animation, 47f atrial perspective, 32f, 04f, 46f chordae tendineae rupture, 52/ in diastole, 44/ full volume, 0f, 5/ imaging techniques, 2-5 3, 5f, 6/ midesophageal views, 03f, 47/ prolapse, 53/ prosthetic, 11 , 3/ quantitative, 3, 6/ repaired, 4/ stenotic, 68, 68/ zoom, 508/ prosthetic valves, 247, 25 f, 252/ pulmonic valve, 8-5 tricuspid valve, 8, 8/ Thromboembolism, prosthetic valves and, 259 Thrombus in critical illness, 478 in dilated carcliomyopathy, 388-389 eustachian valve entrapment of, 444, 444/ before heart transplantation, 388-389 heterogenous, 445, 445/ left heart, LVAD placement and, 395, 396/ left ventricular, 445, 445f left ventricular apical, 9, 320f, 389 in liver transplantation reperfusion phase, 47 , 47 1/ mimicking cardiac tumors, 444-445, 445/ PICC line, 480, 480/ in prosthetic valves, 258-259, 260/ Tilting disk prosthetic valves, 24 -242, 24 1f, 247f, 249-250, 249f Time gain compensation (TGC), Tissue Doppler imaging (TDI) in constrictive pericarclitis, 35 5-356 versus conventional ultrasound techniques, 280 mitral annulus, 280-283, 28 -282/ principles, 280 for strain rate calculation, 526-527, 526f strengths and weaknesses, 66-67 tricuspid annulus, 1 , t for ventricular function assessment, 34-1 35, 5/ I N D EX Toronto SPV stemless biologic valve, 244, 244/ Trabeculations, Transducers, 3-4, 4f, t Transesophageal echocardiography (TEE) complications and safety, 542, 545-548, 546t, 547t contraindications, 545 contrast-enhanced See Contrast-enhanced TEE in critical care See Critical care, TEE in database management, 549 in emergency care See Emergency care, TEE in image acquisition, storage, and retrieval, 548-549 image display, 89-9 I , 90f indications for use, 87, 88t, 463 t, 543-545, 544t midesophageal views See Midesophageal views in noncardiac surgery acute hemodynamic compensation, 462-463, 463t, 464/ l iver transplantation, 470-47 , 471/ lung transplantation, 468-470, 469f monitoring See Monitoring, with TEE patient preparation, 54 -542 peri operative See Perioperative TEE in pregnancy, 47 probe insertion, 87, 542-543 probe manipulation, 87-89, 89f, 90f three-dimensional See Three-dimensional TEE tomographic vie\'ITS, I , 92/ See also Midesophageal views; Transgastric views windows for, 88, 88f Transgasrric views, 92f, 572/ aortic valve deep long-axis, 08, l l Of, 1 1f, 99, 99/ long-axis, 08, 09f, l l 1f, 98-1 99, 99/ left ventricle apical short-axis, 94, 97f, 98f, 99 basal short-axis, 94, 96/ mid short-axis, 94, 97f two-chamber, 99, 1/ mitral valve basal short-axis, 96f, 02, 47-1 48, 48/ two-chamber, 04, 47, 47f, 48/ right ventricle deep, 302 303, 303/ hepatic vein flow, 303, 303/ inflow-outflow, I 4, 1 4f, 1 6f, 301 -302, 302f, 303/ midesophageal four-chamber, 1 short-axis, 30 , 302/ tricuspid valve, 1 deep right ventricular outflow, 233 right ventricular inflow-outflow, 1 4, 1 6f, 222, 225f, 232 short-axis, 222, 226/ Transmittal Doppler flow See Mitral inflow Transmittal velocity proftl e See Mitral inflow Transplant surgery, TEE in heart See Heart transplantation l lver, 470-47 , 471/ lung, 468-470, 469/ Transposition of the great arteries, 428-429, 429f Transverse sinus, 45, 45f, Tricuspid annular plane systolic excursion (TAPSE), 306, 306t, 307f Tricuspid regurgitation after heart transplantation, 392 in dilated cardiomyopathy, 323 etiologies, 223, 223t LVAD placement and, 395 severity assessment, 228t, 584t TEE assessment coronary sin us flow patterns, 227, 229f Doppler evaluation, 226, 227f, 228f, 228 t, 306, 307/ I 64 Tricuspid regurgitation, TEE assessment ( Cont.): hepatic venous flow patterns, 226-227, 229/ systolic pulmonary artery pressure, 227-230, 230/ two-dimensional, 223-225, 227f, 228t Tricuspid stenosis etiologies, 223t, 230 severity assessment, 232t, 584t TEE assessment Doppler evaluation, 23 , 231f, 232t two-dimensional, 230-23 , 23 1f, 232t Tricuspid valve anatomy, 222, 224/ Ebstein's anomaly, 223, 223 t, 224, 7-4 8, 8/ flow recordings, 286 inflow velocities, 0-3 1 , 31 1f, 2t, 322 reference values, 578t regurgitation See Tricuspid regurgitation replacement, 255-256 stenosis See Tricuspid stenosis TEE assessment, I 3f, 11 midesophageal four-chamber view, 222, 224/ midesophageal right ventricular inflow-outflow view, 222, 225f transgastric right ventricular inflow view, 1 6f, 222, 225f transgastric short-axis view, 222, 226f three-dimensional echocardiography, 8, 8f tissue Doppler analysis, 1 , 2t Tricuspid valve area, 584t Tricuspid valve replacement, 255-256 Truncus arteriosus, 428 Two-dimensional echocardiography, resolution, 5-6, 6/ system controls, 6, t annotation, 32 compression, I 9-20, 20/ depth, 22, 22/ focal zone, 22 freeze, 29-30 frequency, 20-2 , 1/ gain, 6, 8, 9/ harmonics, -22, 1/ lateral gain compensation, measurement, 30-32 power, 20 sector size, 22, 23f time/depth gain compensation, zoom, 29, 30/ u Ultrasound See also Doppler ultrasound bioeffects, componentS of system, 4-5 contrast-enhanced See Contrast-enhanced ultrasonography modes of display, propagation through tissues, 2-3 pulsed, 2, 2/ waves, characteristics of, -2, 2/ Ultrasound artifactS, 36, -52 degraded images, 47-48, 47/ falsely perceived objects, 48 ghosting, 50 lateral resolution, 46 longitudinal resolution, 46 mirror image, 48f, 58, 58/ misregistered locations, 48-50, 48f, 49f, 50/ missing srructures, 46, 46f, 47/ refraction, 48, 48/ reverberation, 47-48, 47f, 48f stitch, in 3D i maging, , 1/ I N D EX 642 Ventricular syscol ic fu ncti on ( Cont.) : Ultrasound system trols for color-flow Doppler, mach ine preparation, 22-25, 24J 25f, 25t 16 for pulsed-wave and continuous-wave Doppler, l eft 25-29, 26f, 27f, 28J 29f, 0f, l t for two-dimensional imaging, 6-22, 7-1 8J 7t, 29, 30/ Un iventricular hearr, See Left ventricular syscolic function See Right ventricular systolic function Visceral situs, 406 right 427-428 w Wal l motion abnormilities in critical ly ill patients, 477 in donor hearts, 388 99 v l eft ventricular, Variance map, nonischemic causes, Vector array, scoring, 23, 24/ 5t Velocity acceleration, 69-70, 70/ Velocity map, 23, 24/ Velocity-time integral, 308, 309f Vena contracta i n aortic regurgitation, 208, 1f, 579 t in mitral regurgitation, 579 t TEE assessment, 47f, 5, 57/ i n tricusp id regurgitation, 226 Venae cordis m i n i mae, 423 Ventricle See Left ventricle (LV) ; Right ventricle (RV) Ventricular septal defect, 3-4 5, 3f, 4f, 5/ Ventricular shunt, 68 Ventricular systouc function 465, 465 t 574 t TEE assessment, 477 TEE versus ECG for detection of, Wal l mess, 32, 586 Warfarin (Coumadin) ridge, Wavel ength, I , 42, 42f, 08, 1 1/ 2/ Wessex scented biologic valve, X XPlane imagi ng, X7-2 t transducer, z 465-466 597 t 507, 507f See also Three-di mensional TEE 507, 507f See also Three-dimensional TEE Zoom control, ultrasound systems, 29, 1/ ... Surgery 9 82; 92( 6) : 1 8- 1 34 26 Laas J, Jurmann MJ, Heinemann M, Borst HG Advances in aortic arch surgery Ann Thorac Surg 9 92; 53 (2) :22 7 -23 2 27 Glower DD, Fann JI, Speier RH, et a! Comparison of medical... American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists; endorsed by the Society of Thoracic Surgeons J Am Soc Echocardiogr 20 07 ;20 ( 1 ) : 22 7- 23 coronary artery... quality oflife and high rates of morbidity and mortality At the age of 40, the life­ time risk of developing heart failure is 20 %, and the -year heart failure mortality rate is 20 % The num­ ber of

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