The importance of right ventricular (RV) function in cardiac surgery has been recognized for several years. Many studies have, in fact, demonstrated its prognostic value after valvular heart surgery, coronary artery bypass surgery, heart transplantation, and left ventricular (LV) assist device insertion.1,2 Severe refractory RV failure requiring prolonged inotropic support or RV assist device insertion occurs in approximately 0.1% of patients after cardiotomy, in 2%–3% of patients after heart transplantation, and in 20%–30% of patients receiving a LV assist device.2 The survival rate associated with severe RV failure may be as low as 25%–30%.2 This highlights the importance of early diagnosis as well as better preventive and management strategies. In the perioperative and intensive care setting, echocardiography is becoming the mainstay in the assessment of RV function.
We have recently reviewed the role of the RV in cardiovascular disease.3,4 In this article, we will review RV function from the perspective of the surgeon and anesthesiologist caring for the perioperative patient undergoing cardiac surgery. We will discuss perioperative assessment of RV function, whereas the companion review focuses on the clinical importance of RV dysfunction and on perioperative management.
The anatomy of the RV is both unique and complex. The RV appears triangular when viewed laterally, whereas in cross-section, it appears crescent shaped.5 Although the RV appears smaller than the LV in the four-chamber view, RV volume is, in fact, larger than the LV volume. Based on magnetic resonance imaging, the normal range of RV end-diastolic volume (RVEDV) is 49–101 mL/m2 (males, 55–105 mL/m2; females, 48–87 mL/m2), whereas the normal range of LV end-diastolic volume is 44–89 mL/m2 (males, 47–92 mL/m2; females, 41–81 mL/m2).6,7 In the normal adult, RV mass is also only about one-sixth that of LV mass.1 In childhood, there is a progressive regression of RV hypertrophy as pulmonary vascular resistance (PVR) decreases.
Traditionally, the RV has been divided into two components: the sinus (inflow) and the conus (infundibulum). The RV sinus extends from the tricuspid valve (inflow region) and includes the trabeculated (apical) portion of the ventricle (Fig. 1). The RV conus is usually free of muscular trabeculations and extends from the septomarginal band to the pulmonary valve (arterial trunk). In the anatomic LV, subaortic conal absorption occurs, which explains the absence of an infundibular portion.1 Three prominent muscular bands divide the RV: the parietal, the septal and the moderator band. The parietal band and the infundibular septum make-up the crista supraventricularis, which separates the sinus and the conus regions.8 The moderator band extends from the base of the anterior papillary muscle to the ventricular septum.8
In the study of complex congenital heart disease (CHD), it may be more useful to divide the RV into three parts: an inflow region, the trabeculated apical myocardium, and the outflow region (infundibulum) (Fig. 1).9 In hearts with congenital malformations, one or more of the three components may be rudimentary or absent.9Table 1 summarizes key anatomical and physiological features of the RV and LV.
The primary function of the RV is to receive systemic venous return and pump it into the pulmonary system. Under normal conditions the RV, in contrast to the LV, is coupled to a low pressure, highly distensible arterial system.1,3
The RV is normally connected in series with the LV. In the absence of shunt physiology or significant valvular regurgitation, the stroke volume of the RV will normally match that of the left. Because of the greater end-diastolic volume of the right ventricle, RV ejection fraction (RVEF) is lower than the left. The lower limit of normal RVEF ranges from 40% to 45% compared with 50%–55% for LV ejection fraction.7,10–12 Several mechanisms contribute to RV ejection, the most important being the bellows-like inward movement of the free wall. Other important mechanisms include the contraction of the longitudinal fibers, shortening of the long axis, drawing the tricuspid annulus toward the apex, and the traction on the free RV wall at its points of attachment to the LV as a result of LV contraction.5 In contrast to the LV, twisting and rotational movements do not contribute significantly to RV contraction.13 Furthermore, the contraction of the RV is also sequential, starting with the trabeculated myocardium and ending with the contraction of the infundibulum (normally separated by approximately 25–50 ms).1,14
To better understand the complex relationship between RV contractility, preload, and afterload, many investigators have studied the pressure-volume relationship of the RV (Fig. 2). One of their major findings was that the RV follows a time-varying elastance model in which ventricular elastance is described by the relationship between systolic pressure and volume under variable loading conditions.14–16 Many studies have shown that RV elastance may also be approximated by a linear relationship.1
RV maximal elastance is considered by many investigators to be the most reliable index of RV contractility.1 RV systolic elastance is lower than that of the LV. This arrangement implies that the RV is far more sensitive to increases in afterload.16,17 This can be illustrated in the acute setting, where RV stroke volume decreases significantly after an increase in pulmonary arterial pressure (Fig. 3).1,3,18
The pulmonary circulation is an important determinant of RV afterload. The pulmonary vascular bed is a highly compliant, low-pressure, low-resistance system. In the presence of normal pulmonary circulation, the RV performs approximately one-fourth of the LV stroke work.5 Several factors modulate PVR, including hypoxia, hypercarbia, cardiac output, pulmonary volume and pressure, and specific molecular pathways, most prominent being the nitric oxide pathway (vasodilation), the prostaglandin pathway (vasodilation), and the endothelin pathway (vasoconstriction).1,3,19 Pulmonary vessels constrict with hypoxia (Euler-Liljestrand reflex) and relax in the presence of hyperoxia.20 In some instances, hypercarbia may also be a strong pulmonary vasoconstrictor.
Lung volumes have a differential effect on intra- and extraalveolar vessels which accounts for the unique U-shaped relationship between lung volume and PVR. PVR is minimal at functional residual capacity and increased at large and small lung volumes alike (Fig. 4), this may be observed clinically when hyperinflation of the lungs greatly increases PVR.20 Application of high levels of positive end-expiratory pressure may narrow the capillaries in the well ventilated lung areas and divert flow to less well ventilated or nonventilated areas, potentially leading to hypoxia. An increase in cardiac output distends open vessels and may recruit previously closed vessels decreasing PVR. Regional blood flow to the lungs is also influenced by gravity, where pulmonary blood flow is greater in the dependant areas of the lung.
Ventricular interdependence refers to the concept that through direct mechanical interactions the size, shape, and compliance of one ventricle may affect the size, shape, and pressure-volume relationship of the other.21 The main anatomical determinants for ventricular interdependence include the ventricular septum, the pericardium, and continuity between myocardial fibers of the RV and LV. Ventricular interdependence may occur in both systole and diastole. Although always present, ventricular interdependence is most evident with changes in loading conditions, such as those observed during respiration or sudden postural changes.1,3,21 Ventricular interdependence also plays an important part in the pathophysiology of RV dysfunction.
PERIOPERATIVE ASSESSMENT OF THE RV
In cardiac surgery, right heart catheterization and echocardiography play an essential and complementary role in the assessment of RV structure and function. Both techniques provide useful information that may help tailor the anesthetic and surgical approach and provide guidance in the management of hemodynamically unstable patients. Hemodynamically, RV dysfunction or failure is usually recognized in the presence of a right atrial pressure (RAP) ≥8–10 mm Hg or a RAP to pulmonary capillary wedge pressure ≥0.8 (isolated RV failure) and/or a low cardiac index (≤2.2 L · min−1 · m−2).22,23 Increasing RAP may also be a sign of impeding RV failure. Significant RV outflow tract (RVOT) obstruction may also be suspected in the presence of RV-pulmonary artery gradient more than 25 mm Hg. As will be reviewed in this section, echocardiography also provides useful information on RV and pulmonary structure, valvular function and pericardial physiology. Four recently published guidelines may help to guide the echocardiographic assessment of the RV: 1) ASE/ SCA (American Society of Echocardiography/Society of Cardiovascular Anesthesiologists) guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography (TEE) examination; 2) ASE/SCA guidelines for a comprehensive epicardial echocardiography examination; 3) the ASE and European Association of Echocardiography guidelines on two-dimensional (2D) chamber quantification; and 4) the ASE recommendations for evaluation of the severity of native valvular regurgitation with 2D and Doppler echocardiography.12,24–26
Echocardiographic Views of the RV
In the operating room, both TEE and epicardial echocardiography are helpful in obtaining images of the RV. In the intensive care unit, TEE and transthoracic echocardiography (TTE) constitute useful modalities.
The most useful transesophageal views are illustrated in Figure 5.24 The midesophageal four-chamber view is ideal for visualizing the RV lateral wall and measuring RV internal dimensions and RV fractional area change (RVFAC) (Videos 1 and 2; please see video clips available at www.anesthesia-analgesia.org). The midesophageal views are also useful in visualizing the coronary sinus (Fig. 6), assessing tricuspid regurgitation (usually achieved at an angle of 30°–60°), and assessing potential atrial or ventricular septal defects. The transgastric views allow short-axis views (SAX) of the RV and septum, and views of the RV inflow tract and RVOT, inferior vena cava (IVC) as well as hepatic veins. The anterior and inferior walls of the RV are best visualized in the transgastric views. The great vessels are best studied in the upper esophageal views, whereas tricuspid annular tissue Doppler signals are best assessed in the deep transgastric RV views.
Epicardial echocardiography may be very helpful in the presence of a contraindication to TEE such as an esophageal stenosis, if the images obtained by TEE are suboptimal, for diagnosis of pulmonic valve pathology or for detection of intraoperative thromboembolism.27,28 Most of the imaging planes from TEE can be obtained using epicardial echocardiography (Fig. 7). However, the four recommended ASE views which provide helpful images of the RV include 1) the epicardial aortic valve (AoV) SAX view (TTE parasternal AoV SAX equivalent) (Fig. 7B, Video 3; please see video clips available at www.anesthesia-analgesia.org); 2) the epicardial LV long-axis (LAX) view (TTE parasternal LAX equivalent) (Fig. 7C, Video 4; please see video clips available at www.anesthesia-analgesia.org); and 3) the epicardial LV basal SAX view (TTE modified parasternal mitral valve basal SAX equivalent) (Fig. 7D); and 4) the epicardial RVOT view (TTE parasternal SAX equivalent) (Fig. 7E). Guidelines on this topic were published in 2007.26
Challenges in the Echocardiographic Study of the RV
The echocardiographic study of the RV is more challenging than that of the left. The main difficulties encountered may be explained by 1) the complex shape of the RV, 2) heavy apical trabeculations of the RV, which limits endocardial surface recognition, and 3) the marked load dependence of several indices of RV function.5 Despite these limitations, a comprehensive assessment of the RV may provide important insights into its contractility, preload, and afterload.
Identifying the Anatomic RV
Although the RV is usually on the right side of the heart and connects with the pulmonary artery, the anatomic RV is defined by its structure not by its position or connections. Features which help differentiate the anatomic RV from anatomic LV include 1) the more apical insertion point of the septal leaflet of the tricuspid valve relative to the anterior leaflet of the mitral valve, 2) the presence of a moderator band, 3) the presence of more than 2 papillary muscles, and 4) the trileaflet configuration of the tricuspid valve.1,29,30 This is especially important in CHD, where the anatomic RV may be positioned on the left side of the heart or connect to the aorta.3,30 In a corrected transposition of the great vessels (l-TGA), the anatomic RV is positioned on the left side of the heart and connects to the aorta (systemic ventricle). In a d-transposition of great arteries (d-TGA), the anatomic RV is positioned to the right side of the heart and connects to the aorta. Alternatively, the LV may show more pronounced trabeculations, which may mimic the structure of the anatomic RV (noncompaction of the LV).
RV Size and Shape
Because the complex shape of the RV does not lend itself to simple mathematical modeling, the assessment of RV size using 2D echocardiography remains challenging. The best correlations between 2D echocardiography and RV volumes have been obtained using the maximal SAX dimension and the RV area measured in the four-chamber view (Fig. 8).5,12,31 It is, however, important to note that there is significant overlap between normal patients and patients with RV volume overload.12 Furthermore, normal 2D values have not been well established in patients requiring mechanical ventilation. The availability of 3D TEE technology may in the future allow better intraoperative assessment of RV volumes. At this time, however, software used for RV volume quantification is not routinely available. Figure 9 illustrates normal values of RVOT measurements.
RV hypertrophy is echocardiographically defined as a ventricular wall thickness more than 5 mm at end-diastole. The inferior or lateral walls of the RV are the preferred locations for measurement since, in contrast to the anterior wall, they are not invested with as much epicardial fat.32 The inferior wall of the RV is best assessed in transgastric views performed at 0°, whereas the RV lateral wall is best measured in the four-chamber view. Because the RV wall is thinner and more trabeculated than the LV wall, precise measurements are more difficult to obtain.
The RV shape cannot be described by one simple geometric shape. Under normal conditions, the RV appears triangular, when viewed from the side and crescentic in cross-section.5 The analysis of septal curvature may provide useful insights into RV pathology. The interventricular septum is usually curved (convex) toward the RV (Fig. 10). The eccentricity index, a measure of septal curvature, represents the ratio of the LV minor axis diameter (parallel to the septum) to its perpendicular axis.33,34 In normal subjects, the index is essentially one at both end-diastole and end-systole. In the adult with acquired pressure overload, the RV dilates early and the ventricular septum is displaced toward the LV cavity especially at end-systole. This will distort both RV and LV geometry (D-shaped LV; eccentricity index >1).30 In volume overloaded states, the RV is dilated and rotated clockwise (apical reference). The RV initial crescentic shape is transformed into a more cylindrical configuration, and the ventricular septum is displaced toward the LV cavity (D-shape LV; eccentricity index >1), mainly at end-diastole.30 In patients with congenital pulmonary stenosis, the RV has a greater hypertrophic response, and its shape is more elliptic; dilation occurs late in the course of the disease or in the presence of a critical stenosis. When aneurysms are seen in the RV, the possibility of arrhythmogenic RV dysplasia must be considered. In this condition, the aneurysms occur most commonly in the anterior infundibulum, basal inferior wall, and apex. Other causes of RV aneurysms include myocardial infarction and, in rare cases, absence of a right pericardium.35,36
Indices of RV Function
The study of RV function comprises indices that reflect RV systolic function, RV diastolic function, global and regional RV function, (systole and diastole) and valvular function.37,38 The study of RV dyssynchrony is a new field of research and could play a larger role in the future. Indices of RV systolic function may describe the extent of RV contraction or reflect RV contractility (i.e., the intrinsic ability of the ventricle to contract). An ideal index of contractility would be independent of afterload and preload, sensitive to change in inotropic state, independent of heart size and mass, easy and safe to apply, and proven to be useful in the clinical setting.39 The most commonly used echocardiographic indices of RV systolic function are summarized in Tables 2 and 3 and include
- Geometric indices, those which reflect the extent of contraction, such as RVFAC, RVEF, and tricuspid annular plane systolic excursion (TAPSE).
- Myocardial velocity indices, such as the tricuspid annular plane maximal systolic velocity and the isovolumic acceleration (IVA).
- Hemodynamic indices, such as the RV first derivative of pressure and time (RV dP/dt).
- Time interval indices, such as the RV myocardial performance index (RVMPI) or Tei index which reflect both systolic and diastolic parameters.
Indices of RV Systolic Function
RVEF represents the ratio of stroke volume to end-diastolic RV volume ([RVEDV-RVESV]/RVEDV). RVEF has the advantage of being a widely accepted and validated index of RV function. Its prognostic value has been proven in heart failure, valvular heart disease, and CHD.3 RVEF has, however, the disadvantage of being highly load dependent and may not always reflect ventricular contractility in volume or pressure overloaded states. An accurate assessment of RVEF using echocardiography also remains difficult because of the complex shape and heavy trabeculations of the RV. In 2D echocardiography, RVEF may be assessed using Simpson’s rule or the area length method.40 Because of the complex geometry of the RV and limited RV endocardial definition, reliable estimates of RVEF using 2D echocardiography remain elusive. In the future, 3D acquisition protocols may provide more accurate assessments of RV volume and RVEF.41
Echo-derived RVFAC is an index of RV systolic function that is easier to measure. RVFAC represents the ratio of RV systolic area change to the end-diastolic area. It is measured in the four-chamber view and can be systematically incorporated into a basic echocardiographic study (Fig. 11). In nonsegmental disease, a good correlation has been reported between RVFAC and RVEF measured using magnetic resonance imaging.42 A consensus from the American and European Societies of Echocardiography has determined the ranges in the evaluation of RVFAC: normal values are between 32% and 60%, mildly abnormal between 25% and 31%, moderately abnormal between 18% and 24%, and severely abnormal below 17%.12
TAPSE measures the longitudinal systolic motion of the free edge of the tricuspid valve annulus.43 It is measured using M-mode imaging in the four-chamber view,44 typically on the lateral annulus, although some authors have used the inferior annulus and obtained similar values45 (Fig. 11, Videos 5a and 5b; please see video clips available at www.anesthesia-analgesia.org). Most of the studies using TAPSE were done using TTE. Compared with RVEF and RVFAC, TAPSE has the advantage of not being limited by RV endocardial border recognition. Preoperatively, it may represent a reasonable index of global systolic function; however, its reliability postoperatively has not been as well established.3
Systolic tissue Doppler velocity of the tricuspid annulus (St) has been studied as an index of RV function using both spectral pulsed wave tissue Doppler and color tissue Doppler (Fig. 12, Video 6; please see video clips available at www.anesthesia-analgesia.org). In patients with heart failure, a moderate correlation was noted between St velocity and RVEF (r = 0.65, P < 0.001).46 Currently, its predictive value in cardiac surgery is not well established.
The IVA is a recently described index of systolic performance that is relatively load independent. It is calculated by dividing the maximal isovolumic myocardial velocity by the time to peak velocity using spectral pulsed wave or color tissue Doppler (Fig. 13). In 2002, Vogel et al. used color tissue Doppler to study tricuspid annular IVA in a closed chest animal model during modulation of preload, afterload, contractility, and heart rate. Their study demonstrated that, of all myocardial velocity parameters, IVA was the most reliable noninvasive index of contractility. Three clinical studies confirmed its value in CHD, i.e., postrepair of tetralogy of Fallot (TOF), TGA, and after cardiac surgery.47–50 Further validation of this promising new index in cardiac surgery is, however, required.
The maximum first derivative of RV pressure development (dP/dt max) has also been used as an index of RV contractility. This index may be calculated using continuous-wave Doppler of the tricuspid valve and the Bernoulli equation to calculate the pressure difference from 1 m/s to 2 m/s. Obtaining a reliable signal of tricuspid regurgitation in TEE, however, may be more difficult than in TTE. Furthermore, it has been demonstrated, in numerous studies, that RV dP/dtmax is significantly affected by loading conditions and cannot be used as a reliable index of contractility.51 It may, however, be useful in assessing directional changes in response to therapy, assuming stable loading conditions.
The RVMPI has been described as a nongeometric index of global ventricular function (Fig. 14).52 It represents the ratio of isovolumic time intervals to ventricular ejection time (ET) and is calculated as MPI = (IVCT + IVRT)/ET, where IVCT is the isovolumic contraction time, and IVRT is isovolumic relaxation time.52 RVMPI increases in the presence of systolic or diastolic dysfunction. RVMPI has been validated in several disease states, including CHD, primary pulmonary hypertension, myocardial infarction, and chronic respiratory disease.53–56 A small prospective study has suggested that RVMPI may be useful in stratifying patients undergoing high-risk valvular surgery.38 It is important to remember that RVMPI is less reliable in the presence of arrhythmias or high-grade atrioventricular block. Pseudonormalization of the RVMPI has also been reported in acute, severe RV myocardial infarction.56
Regional RV Systolic Function
The pattern of regional RV dysfunction may also be helpful in differentiating causes of RV dysfunction. For example, in pulmonary embolism, McConnell et al.57 described a distinct pattern of RV dysfunction characterized by severe hypokinesis of the RV mid-free wall associated with normal contraction of the apical segment (best seen in the four-chamber view). In contrast, in other causes of pulmonary hypertension, apical contraction is often depressed.
Variables of RV Diastolic Function
RV diastolic function has not been as extensively studied as that of the LV. Clinically useful diastolic variables of RV diastolic function include RAP, RV filling profiles, and hepatic vein profiles.58 Compared with LV filling, the velocities across the tricuspid valve are significantly lower than those of the mitral. The tricuspid deceleration time is also longer than mitral deceleration time. Tricuspid filling profiles are usually measured in the mid-esophageal view or the transgastric view with rightward rotation of the probe.
In nonventilated patients, the IVC size and collapse index correlate well with RAP. The collapse index refers to the relative decrease in IVC diameter with inspiration (as with sniffing). An IVC size <2 cm with a collapse index of more than 50% usually corresponds to a RAP <5 mm Hg. A dilated IVC with a collapse index of ≤10% usually corresponds to a RAP of 20 mm Hg. Although correlations in ventilated patients have not been as well validated, studies suggest that the collapse index percentage of the IVC correlates with fluid responsiveness.59
Only a few studies have assessed the importance of RV diastolic filling profiles in cardiac surgery.58,60–62 In a study by Carricart et al.,61 abnormal hepatic venous flow velocities before cardiac surgery were associated with an increased need for vasoactive support after cardiopulmonary bypass. These flow velocities, however, were not shown to be an independent predictor of worse outcome on multivariate analysis. In a study by Denault et al.62, abnormal preoperative RV diastolic profiles were associated with difficult separation from cardiopulmonary bypass. Further studies are needed to validate these findings and to assess the independent value of RV diastolic function in cardiac surgery.
In TOF, a restrictive RV filling profile has been associated with worse outcome early after repair of TOF. A “restrictive RV physiology,” as described in TOF, is characterized by the presence of forward and laminar late diastolic pulmonary flow throughout respiration.30 In the presence of a noncompliant RV, atrial contraction results in an increase in RV pressures exceeding pulmonary pressures, thus resulting in late diastolic pulmonary flow. Early after TOF repair, a restrictive RV pattern, suggestive of a noncompliant ventricle, has been associated with a low cardiac output and longer intensive care stays.30,63 Late after TOF repair, however, restrictive RV physiology counteracts the effects of chronic pulmonary regurgitation and is associated with a smaller RV, shorter QRS duration and increased exercise tolerance.30,64
Ventricular interdependence may be exaggerated in patients with constrictive pericarditis or tamponade physiology, whereas it is usually in the normal range in restrictive disease. Other factors which may increase ventricular interdependence include loading conditions and increased intrathoracic pressures.21 The two most useful features that suggest increased ventricular interdependence include the presence of increased reciprocal respiratory changes in tricuspid and mitral inflow maximal velocity and reciprocal respiratory changes in RV and LV size. These features have mainly been studied in nonventilated patients.
Under normal conditions and spontaneous respiration, the tricuspid inflow maximal velocity increase with inspiration is usually <15%, whereas that of the mitral valve is usually <10%. In constrictive pericarditis, the tricuspid velocity change is often higher than 40%, whereas mitral inflow velocity change with respiration is usually more than 25%. In tamponade, the tricuspid respiratory velocity change is often higher than 85% (increasing with inspiration), whereas that of the mitral valve is usually more than 40% (decreasing with inspiration).65 In contrast, in restrictive physiology, the respiratory changes in tricuspid and mitral velocities are usually not increased and the early filling to atrial contraction ratio is often greater than 2 with a mitral inflow deceleration time of <150 ms. There is usually no abnormal septal motion. It is, however, important to emphasize that restriction, constriction, and tamponade may vary in degree of severity and can also coexist, creating clinical pictures which may sometimes be difficult to sort out.
Valvular Function and RV Inflow Tract and RVOT Gradients
The study of RV function would be incomplete without the assessment of the tricuspid or pulmonary valves function. Tricuspid regurgitation may be primary or, more commonly, secondary to RV dilation or pulmonary hypertension. The most common causes of increased right atrioventricular gradient are tricuspid stenosis, tricuspid valvuloplasty, or a prosthetic tricuspid valve. Significant pulmonary regurgitation is usually seen after TOF repair or as a consequence of severe pulmonary hypertension. Increased transpulmonary (outflow tract) gradients may be caused by pulmonary stenosis, structural or dynamic RVOT obstructions or by increased RV cardiac output. Recently, dynamic RVOT obstruction has been described as a possible cause of hemodynamic instability in cardiac surgery (Fig. 15; Video 7; please see video clips available at www.anesthesia-analgesia.org).62 The guidelines from the ASE for the evaluation of tricuspid and pulmonary regurgitation may be found in a review article published in 2003 by Zoghbi et al.25
Acute RV failure after cardiac surgery remains a major cause of morbidity and mortality. A comprehensive assessment of RV function may improve risk stratification and lead to early management of RV failure. Echocardiography is becoming a mainstay in the assessment of perioperative RV function. Although RV assessment remains challenging, echocardiography offers useful information on RV size, shape, and function. Future advances in 3D echocardiography may further improve the assessment of complex congenital defects and lead to better quantification of RV size and function.
The authors thank Antoinette Paolitto for the help with the manuscript.
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