ASKEP ATRIAL SEPTAL DEFECT (ASD) – SlideShare askep-atrial-septal-defect-asd 12 Apr ASUHAN. Atrial Septal Defect Pada ASDHanya sebagian kecil bayi atau anak dengan ASD besar yang simptomatik dan gejalanya sama seperti pada umumnya. Atrial Septal Defect – Download as Word Doc .doc), PDF File .pdf), Text File .txt) or read online. ppt. An atrial septal defect is an opening in the atrial septum, or dividing wall between the two .. Studi Kasus Asuhan Keperawatan Pada Tn.

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Partitioning of the four-chambered heart requires the proper formation, interaction and fusion of several mesenchymal tissues derived from different precursor populations that together form the atrioventricular mesenchymal complex. This includes the major endocardial cushions and the mesenchymal cap of the septum primum, which are of endocardial origin, and the dorsal mesenchymal protrusion DMPwhich is derived from the Second Heart Field. AVSDs are congenital malformations in which the atria are permitted to communicate due to defective septation between the inferior margin of the septum primum and the atrial surface of the common atrioventricular valve.

For many years, maldevelopment of the endocardial cushions was thought to be the sole etiology of AVSDs. Cardiac septation encompasses a complicated series of events in which structures derived from various precursor populations interact and fuse with one another to functionally and physically separate the different compartments of the four-chambered heart.

Given the complexity of the process it may not be surprising that it is incomplete in a significant portion of the human population. In this review, we describe the anatomy of the atrioventricular AV junction, the origin and fate of tissues involved in septation, and will also discuss cardiac malformations that occur when the septation process goes awry.

The fully formed heart is a midline, four-chambered organ positioned within the middle mediastinum. Its two atria, each of which contains a venous component, a body, an appendage, and an AV valve vestibule, are physically and functionally separated by an atrial septum. The atrial septum is comprised of several components including the septum primum SP anchored by a muscular base and the septum secundum SS Fig.

The muscular base of the septum primum forms the floor, or antero-inferior rim, of the oval fossa while the septum secundum contributes to its superior margin. In Figure 1Aa mature, properly septated heart is depicted. The septum primum green has fused to the septum secundum redresulting in closure of the ostium secundum while interaction of the DMP yellowseptum primum and major endocardial cushions blue results in closure of the ostium primum OP.

In Figure 1Ba patent foramen ovale is illustrated. Here, although the septum primum has not fused to the septum secundum, under normal hemodynamic conditions the two remain in contact to functionally partition the atria. If right atrial pressure were to exceed that of the left atrium, however, right-to-left shunting would result. In Figure 1Can ostium secundum defect OSD is depicted; the flap valve green of the ostium secundum is not of sufficient length to prevent atrial communication.

ASKEP Atrial Septal Defect

Figure 1D depicts an incomplete AVSD, a malformation in which atrial shunting is freely permitted due to persistence of the ostium primum. In the adult heart, the superior and inferior caval veins return de-oxygenated venous blood from systemic circulation to the right atrium whereas the pulmonary vein delivers oxygenated, arterial blood from the pulmonic circulation to the left atrium.

During fetal development, however, gas exchange occurs in the placenta and oxygenated blood is carried back to the fetus through the umbilical vein. After bypassing hepatic circulation via the ductus venosus, oxygenated blood enters the inferior caval vein where it joins, but streams separately from, deoxygenated blood returning from lower portions of the developing fetus Barclay et al. At the junction of the right atrium and the inferior caval vein, a flap of tissue termed the Eustachian valve directs the more dorsally located, oxygenated blood across an interatrial communication termed the foramen ovale.

60271371 Atrial Septal Defect

The superior boundary of this communication is formed by the septum secundum while the septum primum acts as a flap valve of the foramen, allowing unidirectional shunting of oxygenated blood from the right to left atrium. The left ventricle and ascending aorta then deliver this blood to the two tissues with the highest oxygen demand, the developing brain and heart. Shortly after birth and the establishment of pulmonic gas exchange, increased relative left to right atrial pressure pushes the septum primum against the septum secundum.

Once in contact, these two structures fuse, resulting in permanent closure of the foramen ovale and two fully partitioned atria. Thus, the foramen ovale, whether patent or closed, is important for the delivery of oxygenated blood to tissues; the fetal patency of the foramen ovale ensures that vital structures receive blood with a higher oxygen content, while its closure postnatally helps maintain arterial oxygen saturation by preventing the mixture of venous and arterial blood. The presence of a patent foramen ovale PFO does not necessarily imply active communication between the two atrial chambers.

Atrial Septal Defect

In fact, as long as fefect atrial pressure exceeds that of the right atrium and if the flap valve is of sufficient size to cover the boundaries of the oval fossa, the PFO remains functionally closed.

Under certain hemodynamic conditions, however, the PFO may open and thus enable thrombi, air or any other substance to pass from venous to arterial circulation.

It is by this mechanism that a PFO may become pathological and result in conditions such as cryptogenic stroke, migraine with aura, and decompression illness Anzola et al. The clinical course of patients diagnosed with an isolated ostium secundum defect is often benign and may be associated with few, if any, functional limitations.

Larger, more severe ostium secundum defects may lead to right atrial volume overload due to persistent left-to-right shunting and, as a result, increased risk of complications such as atrial fibrillation and pulmonary hypertension Clark and Kugler, ; Engelfriet et al. Eventually, increased pulmonic resistance can cause right-sided pressure to increase; subsequently, blood is shunted from right-to-left Eisenmenger syndrome and systemic oxygenation decreases Engelfriet et al.


The ostium primum defect is a less common, but more severe, possible consequence of aberrant septation. Although interatrial shunting is also observed in ostium primum defects, these malformations are now considered to be part of the family of abnormalities known as atrioventricular septal defects AVSD and therefore, will be discussed in the next section. AVSDs ssptal a spectrum of cardiac malformations and include three subtypes: While all AVSDs are wtrial by a common AV valve, the variants differ with respect to the level at which shunting between chambers is deptal as well as the morphology of the common AV valve Anderson et al.

In transitional AVSDs, fusion of the anterior and posterior bridging leaflets results in a single valvar annulus; however, attachment of these leaflets to the ventricular defsct creates, in effect, two distinct valvar orifices. All three variants generally demonstrate interatrial shunting due to defective septation between the inferior margin of the septum primum and the atrial surface of the common atrioventricular valve; however, shunting at the ventricular level will also be permitted if the bridging leaflets are attached to the leading edge of the atrial septum Anderson et al.

In transitional AVSDs, attachment of the common valve to the ventricular septum assists in separation of the right and left ventricle while in complete AVSDs, shunting at the ventricular level is freely permitted through a defect between the ventricular surface of the askp valve and the interventricular septum Jacobs et al. Within these defects, the size of the ventricles is variable but important in determining whether the patient is a candidate for biventricular surgical repair Bharati and Lev, ; Jegatheeswaran et al.

In balanced AVSDs, both ventricles are appropriately sized while in unbalanced AVSDs, one ventricle is so small that the patient must be managed as having a functionally univentricular heart Bharati and Lev, ; Jegatheeswaran et al. Complete AVSDs may also be classified according to the Rastelli classification system, which is based on the morphology, degree of bridging and chordal attachments of the superior leaflet Rastelli et al.

The clinical presentation of AVSD is not uniform and depends on the size of the defect, the degree of shunting as well as the presence of other malformations. In general, untreated complete AVSD results in congestive heart failure within the first few months of life while the signs and symptoms of incomplete AVSD are subtler and may not manifest until later in life Minich et al.

Management of these defects requires surgical correction, which may be complicated by the presence of other cardiac abnormalities including dysplastic AV valve leaflets, isomeric atrial appendages, and tetralogy of Fallot or double outlet right ventricle Shuhaiber et al. Cardiac septa, including septal defects, asmep occur in the context of a syndrome and in association with other abnormalities Table 1.

Holt-Oram syndrome, which results from mutations in TBX5is characterized by atrial and ventricular septal defects as well as upper limb abnormalities Basson et al. Heterotaxy syndromes, or left-right laterality defects, often include septal defects as well as ayrial of the atrial appendages and may result from dysregulation of pathways involved in left-right patterning, such as PITX2SHH and NODAL Cunningham et al.

The most common genetic syndrome, Down syndrome trisomy 21is strongly associated with defevt septal defect; approximately one-quarter of children with Down syndrome possess this malformation and roughly two-thirds of complete AVSD occur in association with trisomy 21 Barlow et al.

Genetic mutations may also result in non-syndromic septal defects, defects that occur in isolation or in absence of phenotypic features typically associated with a syndrome Table 2. Non-syndromic AVSDs, which are estimated to occur in approximately one defwct 10, live births, are thought to occur as a result of multifactorial inheritance or sporadic mutations Carmi et al.

Between anda large case-control study, the Baltimore-Washington Infant Study, was conducted to assess risk factors for askeo cardiovascular defects.

This study, which included infants with AVSD of whom were also diagnosed with Down syndromeprovided invaluable information regarding the contribution of non-inherited risk factors to the pathogenesis of septal defects.

The results of this study, as well as others, are summarized here and in table 3. Although the mechanism is not fully understood, pre-gestational diabetes significantly increases the risk of askdp syndromic Loffredo et al.

Other potential risk factors for AVSD include urinary tract infection during the first trimester of pregnancy Cleves et al. Ostium secundum defects have been linked to pre-pregnancy obesity Gilboa vefect al. Much like their morphological features, classification, and clinical presentation, the etiology of septal defects is complex. These defects may arise from perturbation of any one component of the AV septal complex and development of each component is governed by multiple molecular pathways.

In the vertebrate embryo, the heart is the first organ atial become functional; its development commences at gastrulation with the formation of precardiac mesoderm. Cells zskep this middle embryonic germ layer then migrate anterolaterally to establish bilateral primary heart fields. The two heart fields eventually combine to form the cardiac crescent and, as the mesodermal cells differentiate into myocardial and endocardial progenitors, the primary heart tube Abu-Issa and Kirby, The linear tube is suspended from the foregut endoderm by the dorsal mesocardium and is oriented such that the arterial pole outflow is cranial to the venous pole inflowwith bilateral venous tributaries draining into the latter Drake et al.

The two poles of the linear tube soon receive contributions from a second cardiogenic population; this population of cells is termed the Second Defecg Field SHF and its addition leads to pronounced arial of the linear tube Kelly and Buckingham, ; Mjaatvedt et al. Soon thereafter, the central portion of dorsal mesocardium suspending the linear tube disintegrates, enabling the primary heart tube to loop to the right Manner, Looping of the primary heart tube results in a more cranially and dorsally positioned inflow region.


This inflow region, or venous pole of the primary heart tube, gives rise to the symmetrical common atrium which receives blood from the developing embryo through bilateral venous tributaries, the right and left superior caval veins.

At this point, the common atrium is separated from the left ventricle by the AV canal but the various components are still arranged in series. Along the outer curve, serial ballooning gives rise to the apical portions of the right and left ventricles Davis, ; Lamers and Moorman, ; Moorman et al.

It is through remodeling events along the inner curvature and at its junction with the AV canal and the outlet component that the atrial cavities come to be shared between ventricles. While the left atrium is able to communicate with the left ventricle from sepal outset, communication between the septql atrium and the right ventricle requires expansion of the AV canal, the right side of which defec incorporated into the right atrium as the vestibule of the tricuspid valve Wessels et al.

Within just one embryonic day in murine development, the atrial entry point of the caval veins shifts from a caudal to dorsal position Soufan et al. The junction between the systemic venous tributaries and the developing right atrium can be visualized by the appearance of the venous valves, bilaminar structures that merge cranially to form the septum dfeect in cefect roof of the right atrium Anderson et al.

Simultaneously, the systemic venous tributaries are enveloped by primary myocardium as they are incorporated into the pericardial cavity Soufan et al. Eventually, the caval veins are further enclosed by primary myocardium and more caudally, canalization of the pulmonary pit leads to communication between the pulmonary vein and atrial cavity Soufan et al.

It should be noted that mouse and man differ with respect to strial venous pole of the heart.

In humans, the left caval vein regresses with the proximal portion giving rise to the coronary sinus while the rest of it forms the ligament of Marshall and the oblique vein Wessels and Sedmera, ; if it fails to do so, persistent left superior caval vein results. In the mouse, however, persistence of the left superior caval vein is normal; the vessel is joined by the azygous vein as well as several cardiac veins before it drains into the right atrium Wessels and Sedmera, The primary heart tube consists of an outer layer of myocardium deect from an inner layer of endocardium by an acellular, extracellular matrix or, cardiac jelly.

The production of lipophilic glycosaminoglycans results in localized formation of AV, or drfect, cushions DeVlaming et al. The endocardial cells lining these cushions are unique in that they respond to growth factors released by underlying myocardium; after receiving these inductive cues, they undergo an epithelial-to-mesenchymal transition EMT and then migrate away from the surface and into the cushions DeVlaming et al. This process of epithelial-to-mesenchymal transition results in the mesenchymalization of the two major endocardial cushions of the AV canal: The two major cushions then expand and eventually fuse, separating the atial into left and right AV orifices.

Following development of the major endocardial cushions, the lateral cushions appear later as lateral swellings of mesenchyme at the junction between the atria and ventricles de Lange et al. Each of the four cushions plays an important role in AV valvuloseptal development; the superior and inferior AV cushions contribute to the aortic atrkal of the mitral valve and the septal leaflet of the tricuspid valve Snarr et al.

The lateral cushions also make significant contributions to the AV valves; the right lateral cushion contributes to the anterosuperior and inferior leaflets of the tricuspid while the left lateral cushion is involved in formation of the mural leaflet of the mitral valve Snarr et al.

Despite their significant contribution to valvuloseptal development, the lateral AV cushions have been largely ignored in most experimental studies and thus, relatively little is known regarding the molecular mechanisms that govern their delayed formation and maturation.

Further studies comparing development of the major and lateral cushions are certainly needed as recent work indicates that the two are fundamentally different Wessels et al.

Proper formation of the major cushions, which are centrally located between the interventricular septum and interatrial septum, is critical to cardiac septation as all components of the AV septal complex eventually fuse to these structures. Cushion abnormalities are observed aske; a number of genetically modified mouse models, including neurofibromin-1, retinoid X receptor alpha, and hyaluronan synthase-2 knockout mice Camenisch et al.

While defects of the endocardial cushions are variable with respect to etiology and morphological features, they are usually severe and result in embryonic lethality. The septum primum makes its first appearance in the looped heart as a muscular crescent in the roof of the common atrium.

Laporan Pendahuluan Atrial Septal Defect

This true septal structure is capped on its leading edge by mesenchyme and protrudes into the atrial cavity toward the fusing endocardial cushions Figs. As it proceeds toward the superior and inferior endocardial cushions, the left and right atrial chambers communicate via the ostium primum. Eventually, the mesenchymal cap of the septum primum fuses with the endocardial cushions Fig.

This results in formation of the ostium secundum and the preservation of interatrial communication Figs. Fusion of the septum primum to the AV cushions and concomitant detachment from the roof of the atrial cavity enables the muscular septum primum to act as the flap valve of the oval foramen Figs.