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W2048681702 abstract "The number of adults recognized with congenital heart disease (CHD) has increased dramatically over the past five decades because of significant advances in diagnosis and medical and surgical care. At the moment, the population of adults with CHD (ACHD) in the United States is estimated at approximately one million (1). For the first time, the number of adults with congenital cardiovascular malformations equals the number of children with these disorders. With additional refinements in surgical techniques and definitive repair at an earlier age, this patient group is likely to increase even further. Survival rates in CHD are influenced by many factors, including year of birth, age at diagnosis, complexity of the pathology, and whether the lesion(s) has been palliated or surgically corrected (Table 1) (1). As survival and life expectancy continue to improve, a growing number of unoperated, palliated, and “repaired” individuals require surgical interventions or other procedures related or unrelated to their heart disease. The care of these patients is becoming more frequent in all surgical settings, including tertiary care facilities, ambulatory centers, and labor and delivery suites.Table 1: Survival Rate from Year of Birth (1940–2000) by Complexity of Congenital Heart DiseaseAdults with CHD may come to the attention of anesthesiologists for various indications including: Cardiac surgery for the first time (for either palliation or definitive surgery) Cardiac reoperation for further palliation or definitive correction after palliative surgery Cardiac surgery for management of residua, complications of prior intervention, or conversion of a priori repair to a modern, potentially more favorable, strategy Noncardiac surgery or other nonsurgical procedures in the presence of uncorrected, palliated, or corrected lesions. Anesthesia and surgery may carry an increased risk for adverse events during emergent or elective procedures in these patients. This is particularly the case in those with cyanosis, pulmonary hypertension, rhythm disturbances, and significant hemodynamic abnormalities. Recommendations from organizations such as the American College of Cardiology (1) and the Canadian Cardiovascular Society (2–4) suggest that these patients should be cared for by cardiac anesthesiologists who have specialized training or extensive experience in the field. However, anesthesia care providers with such advanced expertise may not always be available. The challenge in caring for these patients is further magnified by the fact that there is a heterogeneous population. Individuals may present at any time with a bewildering array of structural variations, each with specific physiologic perturbations and hemodynamic consequences, and situations that require sophisticated perioperative care. The spectrum of CHD ranges widely from relatively mild defects seen in isolation to lesions of moderate to severe complexity typically characterized by several coexistent malformations. An important objective in caring for ACHD is to diminish cardiac-related morbidity and avoid adverse perioperative events. Of utmost importance in this mission is having a basic understanding of the native anatomy, physiology, surgical strategies, and late outcome of the defect under consideration. The primary goal of this article is to present a general overview of the most common congenital cardiovascular defects as applied to the adult age group, with a focus on anatomy, physiology, and long-term outcome (Table 2). To facilitate this review, representative images of the various congenital pathologies, as displayed by transesophageal echocardiography (TEE), accompany this contribution. The graphics are accessible as digital clips on the Web site of Anesthesia & Analgesia (www.anesthesia-analgesia.org), and we hope the clips will serve as reference material for those involved in the care of these patients. The images are labeled according to the American Society of Echocardiography/Society of Cardiovascular Anesthesiologists guidelines (5). We have made a significant effort to display most of the echocardiographic images as obtained in the population of focus, the adult patient. This imaging modality has provided significant contributions to the care of patients with structural congenital cardiovascular pathology, and we emphasize the benefits of this technology. The TEE imaging planes and information of interest for each of the lesions considered are listed in Table 3 as a guide to those who may want to become more familiar with the applications of this imaging approach to CHD. Epicardial echocardiography contributed significantly in the early experience of intraoperative imaging in patients with CHD; however, it is used primarily in patients when TEE is not feasible.Table 2: Congenital Heart Disease: Long term OutcomeTable 2: ContinuedTable 2: ContinuedTable 3: Transesophageal Echocardiography (TEE) in the Evaluation of Congenital Heart DiseaseTable 3: ContinuedFor an in-depth review of ACHD and the applications of TEE in these patients, the reader is referred to several comprehensive resources on the subject (6–11). The anesthestic considerations and management issues of CHD are beyond the scope of this article and have been addressed elsewhere (12–15). We have divided this manuscript into a discussion of simple and complex lesions, with “complex” defined as the presence of more than one congenital malformation often requiring surgical intervention. Simple Lesions Atrial Septal Defects (ASD) Anatomy and Physiology. Defects in the interatrial septum or ASDs comprise 7%–10% of all congenital cardiac anomalies (16). These defects account for nearly a third of all structural defects detected in adults, occurring more commonly in female patients than in males (17). Although classification of ASDs is primarily based on their location, characterization of interatrial communications is important in view of the incidence of associated anomalies and their impact on surgical management. Several types of defects are recognized including the following: 1) Ostium secundum or fossa ovalis defect (75% of ASDs) is the result of a deficiency in the septum in the region of the fossa ovalis (near or at the mid-aspect of the interatrial septum). Varying degrees of mitral valve prolapse and/or mitral regurgitation can occur in the adult related to myxomatous degeneration (18–21). 2) Ostium primum defect (15% of ASDs), regarded as a form of atrioventricular septal (canal) defect, involves a deficiency in the inferior aspect of the interatrial septum. Abnormalities of the atrioventricular valves occur most commonly in the form of a commissure or “cleft” in the anterior mitral leaflet potentially accompanied by variable degrees of valvular regurgitation. 3) Sinus venosus defect (10% of ASDs) is usually located in the superior aspect of the atrial septum, inferior to the junction of the superior vena cava and right atrium. This defect, also known as superior vena cava-type of sinus venosus ASD, is more common than its counterpart the inferior vena cava-type of defect (located posteriorly at the inferior vena to right atrial junction). These interatrial communications are frequently associated with anomalous pulmonary venous drainage (80%–90% of cases) from the right lung (22). 4) Coronary sinus defects (relatively rare) consist of a communication between the left atrium and mouth of coronary sinus. These defects are commonly associated with unroofing of the coronary sinus and a persistent left superior vena cava (LSVC) that drains directly into the left atrium (23,24). Other entities that may not be routinely considered in the classification of ASDs but may allow for interatrial shunting include a patent foramen ovale (PFO) at one end of the spectrum (25) and a confluent or common atrium at the other. Patency of the foramen ovale has been reported in as many of 25% of patients (26). In recent years, the presence of a PFO has been associated with the pathogenesis of migraine headaches (27,28). The potential for right-to-left shunting allowed by an incompetent flap of the fossa ovalis may be a risk factor in some patients for paradoxical embolization and cerebrovascular morbidity. A common atrium is characterized by complete or near-complete absence of the interatrial septum and is seen most frequently within the context of complex CHD. A direct communication between the atrial chambers allows for pulmonary venous blood to enter the right atrium. The magnitude of interatrial shunting relates to the size of the defect, relative ventricular compliances, and pulmonary artery pressures. A clinically significant defect results in right-sided volume overload characterized by right atrial, right ventricular, and pulmonary artery dilation. The abnormally increased pulmonary blood flow may be a long-term risk factor for the development of pulmonary vascular changes in a small number of patients (5%–10%). Several factors are considered in evaluating the need for intervention. These include the magnitude of the shunt or pulmonary flow (Qp) to systemic flow (Qs) ratio (also known as Qp:Qs) and concerns regarding the potential detrimental effects of chronic right ventricular volume overload. Further factors that influence the management approach include the presence or potential for atrial arrhythmias, risks for the development of pulmonary hypertension, pulmonary vascular obstructive disease, paradoxical embolization, and right ventricular failure. It is important to recognize that physiologic changes in left ventricular compliance and aging may account for unfavorable increases in the degree of left-to-right shunting, exacerbation of symptomatology, and development of right heart failure in the adult. Long-Term Outcome. Primary suture or patch closure of ASDs during childhood provides excellent operative results and nearly normal long-term survival (29,30). Surgical mortality is rare for isolated secundum defects in the current medical era. However, an increased risk is recognized in older patients and those with more than mild increases in pulmonary vascular resistance. As a rule, younger patients have a better outlook after repair (29–31). However, recent data have demonstrated that ASD closure is beneficial even in patients older than 50 or 60 yr (32). Both retrospective studies and prospective clinical trials suggested improved 10-yr survival in patients older than the age of 40 yr treated surgically (95%) compared with those treated medically (84%) (30,33,34). Atrial arrhythmias may be seen especially after the third decade of life. Late repair, after age 41 yr, does not appear to reduce the incidence of rhythm disorders (29). A management strategy that combined defect closure with arrhythmia surgery (Cox/Maze procedure) has been reported to be of benefit in these patients (35). Closure of these defects by the transcatheter route is becoming a widespread alternative to the surgical approach (36–39). Outcomes appear to be good, with successful closure that is generally safe (40). Minimally invasive surgical techniques using a lateral thoracotomy or limited sternotomy have been developed for patients who are not candidates for interventional device closure. This surgical approach has become an attractive option for patients, with better postoperative recovery and improved cosmetic results (41,42). The development of robotic techniques has helped reduce both incision size and overall postoperative trauma. Closure of ASDs has been performed via an endoscopic approach safely and effectively (43). In this study, quality of life outcome measures were superior in patients who received endoscopic surgery as compared with traditional sternotomy and mini-thoracotomy; however, further outcome studies are needed to evaluate the safety and efficacy of this approach. TEE. The identification and comprehensive characterization of ASDs by transthoracic echocardiography in the adult may be limited in some instances by poor acoustic windows. Transesophageal evaluation should be considered a complementary imaging modality in ascertaining or confirming the presence, size, and location of the defect in these patients. The mid-esophageal (ME) four-chamber and bicaval views are particularly useful in the examination of the atrial septum by two-dimensional imaging and color Doppler (Fig. 1 and Table 3) (see video clips 1–3 at www.anesthesia-analgesia.org). Additional benefits of this technology include assessment of the severity of associated atrioventricular valve regurgitation, chamber enlargement and ventricular function (transesophageal and transgastric views). Concomitant defects such as anomalous pulmonary venous drainage can also be defined by a combination of imaging planes. TEE has been shown to be of benefit during transcatheter closure by assisting in the selection of appropriate devices and monitoring during placement (Fig. 2 and Table 3) (see video clips 4 and 5 at www.anesthesia-analgesia.org) (44). Intraoperative benefits during cardiac procedures include documentation of the adequacy of the repair, exclusion of potential problems related to the intervention, and facilitation of cardiac de-airing. Obstruction to systemic or pulmonary venous flow, as well as erroneous diversion of systemic venous drainage to the left atrium, can be recognized by TEE.Figure 1.: Atrial Septal Defects. Top: Secundum atrial septal defect. Mid-esophageal four-chamber view demonstrating the large interatrial communication, with superior and inferior rims of atrial septal tissue bordering the centrally located defect. Color Doppler interrogation shows predominantly left-to-right shunting. RA = right atrium; RV = right ventricle. Middle: Primum atrial septal defect. Left: Mid-esophageal four-chamber view showing the defect in the inferior aspect of the interatrial septum. Arrow indicates the location of the atrial septal defect. LA = left atrium; LV = left ventricle. Right: Color flow Doppler interrogation demonstrates atrial level left-to-right shunting through the atrial septal defect. Bottom: Sinus venosus atrial septal defect. Mid-esophageal bicaval view showing a large atrial communication at the superior aspect of the interatrial septum, underneath the entrance of the superior vena cava into the right atrium. A dilated right pulmonary artery is shown in its short axis as it courses in perpendicular fashion behind the superior vena cava. RPA = right pulmonary artery; SVC = superior vena cava.Figure 2.: Atrial Septal Defects. Device Closure. Left: Transcatheter closure of atrial septal defect. Foreshortened mid-esophageal four-chamber view obtained during transcatheter closure of a secundum atrial septal defect. The clamshell device (arrow) is noted to be in good position in the interatrial septum. The legs of the device straddle both aspects of the interatrial septum. RA = right atrium. Right: Dislodged clamshell occluder device. Mid-esophageal four-chamber view with probe anteflexion shows an echogenic foreign body in the left ventricle. Embolization of the atrial septal defect occluder device (arrow) resulted in this being dislodged at the tips of the mitral valve leaflets. The patient required emergency surgery for device retrieval and closure of the interatrial communication. LA = left atrium; LV = left ventricle; RV = right ventricle.Color flow mapping contributes to the evaluation of interatrial shunting and atrioventricular valve competency. Contrast echocardiography with agitated saline can enhance the identification of small atrial level shunts, as microbubbles are readily apparent in the left atrium even when a very small number move across the defect (45,46). Ventricular Septal Defects (VSD) Anatomy and Physiology. VSDs are the most common of all congenital cardiac anomalies, excluding a bicuspid aortic valve. Epidemiologic studies suggest that these defects account for nearly 30% (range, 16%–50%) of all cases (47,48). Communications at the ventricular level can be found in isolation or may be seen in the context of other structural malformations. Adults with unoperated VSDs are encountered less frequently than are those with ASDs. Large defects usually require surgical attention during childhood for symptomatology related to congestive heart failure or pulmonary hypertension. Although VSDs have a more frequent rate of spontaneous closure in children (6), small perimembranous and trabecular muscular defects may also completely close spontaneously even in adulthood (6). Various classification schemes have been proposed for VSDs (11,49,50). The classification noted below of four major morphologic types is based on the anatomic location of the defect. However, in some cases the rims of the defect may extend beyond the margin of a particular region of the ventricular septum to another. 1) Perimembranous defects, the most common type (70% of VSDs), are located in the membranous septum, just inferior to the level of the aortic valve. Frequently these defects are associated with tricuspid valve aneurysms or redundant septal tricuspid valve tissue that may restrict flow through or completely occlude the defect. 2) Muscular defects (20% of VSDs) are located anywhere within the trabecular component of the ventricular septum, including the anterior and posterior portions and apical region. Multiple defects can occur, giving the appearance of a “swiss cheese” septum, making surgical closure challenging. 3) Doubly committed or subarterial (also known as supracristal) defects (5% of VSDs) are found in the region that would normally correspond to the subpulmonary infundibulum. Fibrous continuity of the pulmonic and aortic valve is generally present. These defects may have associated aortic cusp deformity or herniation leading to aortic regurgitation (51,52). This results from lack of valvular support by the outlet septum. 4) Inlet defects (5% of VSDs) occur in the posterior portion of the ventricular septum in close proximity to the atrioventricular valves. Associated atrioventricular valve anomalies frequently coexist. Defects that may be found in association with VSDs include a bicuspid aortic valve, aortic coarctation, and right ventricular outflow tract (RVOT) obstruction in the form of pulmonic valve stenosis or anomalous right ventricular muscle bundles. An interventricular communication may also be present in complex forms of CHD and in certain types of single-ventricle type arrangements. These intracardiac communications allow for shunting at the ventricular level. The physiologic consequences of this lesion are determined by the size of the defect, amount of shunting, and relative resistances of the pulmonary and systemic vascular beds. Isolated VSDs are also classified in physiologic terms as either pressure restrictive (right ventricular pressure less than left ventricular pressure) or nonrestrictive defects (equal or near-equal ventricular pressures). If the defect is restrictive the flow across it is usually limited. This is often the case with small defects. If the defect is large and nonrestrictive the magnitude of the shunt is dependent on the ratio between the pulmonary and systemic vascular resistances. A low pulmonary vascular resistance in the context of a nonrestrictive VSD leads to a large left-to-right shunt. The excessive pulmonary blood flow in turn results in increased left ventricular end-diastolic volume. In addition to the classification of VSDs according to their anatomic location or restrictive/nonrestrictive nature, characterization of this malformation in terms of size and likely hemodynamic significance is extremely useful as follows: Small Defect: pulmonary to systemic systolic pressure ratio <0.3 and Qp:Qs <1.4 (53). The defect causes negligible to minimal hemodynamic changes. Normal right ventricular systolic pressure (RVSP), pulmonary vascular resistance, and left ventricular size are typically encountered. Moderate Defect: pulmonary to systemic systolic pressure ratio more than 0.3 and Qp:Qs of 1.4 to 2.2 (54). These lesions may be associated with volume overload and congestive symptoms. Some degree of pulmonary hypertension is typically present, as are left atrial and left ventricular dilation. These defects are less common than smaller defects in the adult. Large Defect: systolic pressure ratio more than 0.3 and Qp:Qs more than 2.2. In most patients a long-standing defect of this magnitude leads to the eventual development of pulmonary vascular obstructive disease (Eisenmenger's syndrome, discussed subsequently). Long-Term Outcome. Surgical closure of VSDs early in childhood results in excellent outcomes with survival into adulthood generally without sequelae (55,56). Surgical intervention in older children may be associated with reduced left ventricular function and increased left ventricular mass (57). Small interventricular communications, although regarded as hemodynamically insignificant, may not be necessarily benign. This has led to continuing controversy regarding the need for surgical intervention. In a long-term follow-up of 188 adults with small defects, spontaneous closure occurred in 10% during adult life; however, serious complications occurred in 25% of this cohort (53). These complications included infectious endocarditis (11%), progressive aortic regurgitation (5%), and symptomatic rhythm disturbances (8.5%), with atrial fibrillation being most common (53). A number of individuals with moderate defects may remain relatively asymptomatic until adult life when gradual decompensation ensues related to ventricular dilation. New York Heart Association functional class more than I, cardiomegaly, and an increased pulmonary artery systolic pressure (>50 mm Hg) are clinical predictors of an adverse prognosis (17). Approximately 10% of patients with nonrestrictive VSDs develop Eisenmenger's syndrome, characterized by pulmonary vascular obstructive disease and reversal in the direction of the ventricular level shunt (6). These patients can survive into adulthood but typically have an overall decreased survival rate. The initial description of the clinical features of what today is known as Eisenmenger's syndrome was made in 1897 (58). Several years later the term “Eisenmenger's complex” was formally coined to include pulmonary hypertension at systemic levels related to increased pulmonary vascular resistance, with reversed or bidirectional shunting through a large VSD (59). This syndrome now describes the physiology associated with obliterative pulmonary vascular changes and cyanosis related to a reversal in the direction of an intracardiac or arterial level shunt. Morbidity in these patients relates to problems associated with chronic cyanosis and erythrocytosis, such as thromboembolic events, cerebrovascular complications, and the hyperviscosity syndrome. Other complications include hemoptysis, gout, cholelithiasis, hypertrophic osteoarthropathy, and decreased renal function. The long-term prognosis for patients with this syndrome is better than in those with other causes of pulmonary vascular pathology, such as primary pulmonary hypertension (60). However, life expectancy is significantly altered, with a reported survival rate of 80% at 10 yr, 77% at 15 yr, and 42% at 25 yr (61). Variables associated with poor outcomes include syncope, increased right ventricular end-diastolic pressure, and significant hypoxemia (systemic arterial oxygen saturation of <85%) (61). Most patients succumb suddenly, probably from ventricular arrhythmias. Patients with Eisenmenger's have undergone combined heart and lung transplantation (62) and lung transplantation alone has evolved as an alternate therapy (63). Surgical closure of VSDs is recommended if the magnitude of the increase in pulmonary vascular resistance is not prohibitive. However, if the ratio of the pulmonary to systemic vascular resistance exceeds 0.7, the risk associated with surgical intervention is significant. In a series of adult patients with VSDs, no postoperative problems were experienced if the resting pulmonary vascular resistance was ≤7.9 U/m2 (Woods units) (64). If postoperative pulmonary hypertension persists, the prognosis is unfavorable, with right ventricular failure occurring commonly (65,66). In patients with defects associated with aortic regurgitation, late results after surgical closure of the defect and concomitant aortic valvuloplasty are generally good. A survival rate of 96% at 10 yr has been reported in young patients, with freedom from valvuloplasty failure and freedom from reoperation documented to be 76% and 85%, respectively, at 10 yr (67). Transcatheter closure has been increasing in popularity (68) for both postoperative residual and muscular VSDs (69–71) with excellent closure rates and infrequent mortality. TEE. The role of TEE in the evaluation of patients with VSDs has been well described (Table 3) (72,73). Transesophageal examination allows for definition of the location and size of the defect and determination of chamber sizes and vessel dimensions, aids in the detection of associated anomalies, and provides for identification of ventricular septal aneurysms if present, in addition to the assessment of the aortic valve for herniation and/or regurgitation (74). Views that allow for a comprehensive examination of the ventricular septum include the ME four-chamber view (with sweeps that span from the anterior [outlet] to the posterior [inlet] aspects) and the transgastric (TG) mid short axis (SAX) view (Figs. 3 and 4 and Table 3) (see video clips 6–9 at www.anesthesia-analgesia.org). Doppler color flow imaging allows for determination of the direction and magnitude of the ventricular shunt and permits identification and quantitation of associated aortic regurgitation. Pulsed and continuous wave Doppler can be used to determine the peak flow velocity across the VSD and to provide an estimate of RVSP and pulmonary artery systolic pressure. In the presence of restriction, the peak velocity across the VSD is high, consistent with a relatively high systolic pressure gradient across the ventricular chambers. In the absence of pulmonary outflow tract obstruction the peak velocity across the VSD as determined by spectral Doppler can be used to predict RVSP according to the modified Bernoulli equation as follows (75): Figure 3.: Ventricular Septal Defects. Top: Perimembranous ventricular septal defect. Left: Mid-esophageal four-chamber view demonstrating a deficiency in the membranous septum consistent with a perimembranous ventricular septal defect. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. Right: Color Doppler interrogation across the defect documents left-to-right shunting. Bottom: Supracristal ventricular septal defect. Left: Mid-esophageal aortic long axis view showing a subarterial ventricular septal defect. The close relationship of this defect to the semilunar valves is noted. Right: Color Doppler demonstrates ventricular level shunting.Figure 4.: Ventricular Septal Defects. Left: Muscular ventricular septal defect. Mid-esophageal four-chamber view post-cardiopulmonary bypass showing left-to-right shunting through a small residual muscular ventricular septal defect at the inferior aspect of the patch (arrow). LV = left ventricle; RV = right ventricle. Middle: Inlet/Muscular ventricular septal defect. Mid-esophageal four-chamber view demonstrating a large inlet muscular ventricular septal defect below the level of the atrioventricular valves. Right: Mid-esophageal four-chamber view with color flow Doppler showing left to right ventricular shunting." @default.
W2048681702 created "2016-06-24" @default.
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W2048681702 date "2006-03-01" @default.
W2048681702 modified "2023-10-14" @default.
W2048681702 title "Congenital Heart Disease in the Adult: A Review with Internet-Accessible Transesophageal Echocardiographic Images" @default.
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