{{Infobox_Disease |
  Name           = Atrial septal defect |
  Image          = Gray468.png |
  Caption        = Heart of human embryo of about thirty-five days |
  Width          = 350 |
  DiseasesDB     = 1089 |
  ICD10          =  |
  ICD9           = - |
  ICDO           = |
  OMIM           = 108800 |
  MedlinePlus    = |
  eMedicineSubj  = med |
  eMedicineTopic = 3519 |
  MeshName       = Atrial+Septal+Defects |
  MeshNumber     = C14.240.400.560.375 |
}}

'''Atrial septal defect''' ('''ASD''') is a form of congenital heart defect that enables blood flow between the left and right atria via the right and left atria.  Without this septum, or if there is a defect in this septum, it is possible for blood to travel from the left side of the heart to the right side of the heart, or vice versa. Irrespective of interatrial communication bi-directions, this results in the mixing of arterial and venous blood. The mixing of arterial and venous blood may or may not be hemodynamically significant, if even clinically significant. This mixture of blood, may or may not result in what is known as a "Shunt". The amount of shunting present, if any, dictates hemodynamic significance. (See Pathophysiology below). It should be noted however, that a "Right-to-left-shunt" typically poses the more dangerous scenario (See Pathophysiology below).

The right side of the heart contains venous arterial blood with a high oxygen content. The construction of a heart void of an ASD prevents interatrial communication by means of an uncompromised interatrial septum. This prevents the atria from regular communication with each other, and thus oxygen rich blood and oxygen deficient blood do not mix together properly.

During development of the left and right atria.  The ''foramen ovale'' () remains open during fetal development to allow blood from the venous system to bypass the lungs directly and enter the circulatory system.  This is so, as prior to birth, the oxygenation of the blood is provided via the mother's placenta as the lungs of the fetus are not breathing air. A layer of tissue begins to cover the foramen ovale during fetal development, in which typically, after birth, the pressure in the pulmonary circulatory system drops, thus causing the foramen ovale to close entirely. In approximately 25% of adults, the foramen ovale does not entirely seal.  In this case, elevation of pressure in the pulmonary circulatory system (ie: pulmonary hypertension due to various causes, or transiently during a cough) can cause the foramen ovale to remain open.  This is known as a '''patent foramen ovale''' ('''PFO''').

==Pathophysiology==
thumb|250px|Atrial septal defect with left-to-right shunt
In unaffected individuals, the chambers of the left side of the heart make up a higher pressure system than the chambers of the right side of the heart.  This is because the left ventricle has to produce enough pressure to pump blood throughout the entire body, while the right ventricle only has to produce enough pressure to pump blood to the lungs.

In the case of a large ASD (>9mm), which may result in a clinically remarkable ''left-to-right shunt'', blood will shunt from the left atrium to the right atrium causing excessive interatrial communication (In the case of hemodynamically significant ASD (Qp:Qs > 1.5:1), the patient is often found to be notably symptomatic and ASD repair may be indicated). This extra blood from the left atrium may cause a volume overload of both the right atrium and the right ventricle, which if left untreated, can result in enlargement of the right side of the heart and ultimately heart failure.

Any process that increases the pressure in the left ventricle can cause worsening of the left-to-right shunt.  This includes hypertension, which increases the pressure that the left ventricle has to generate in order to open the aortic valve during ventricular systole, and coronary artery disease which increases the stiffness of the left ventricle, thereby increasing the filling pressure of the left ventricle during ventricular diastole.

The right ventricle will have to push out more blood than the left ventricle due to the left-to-right shunt.  This constant overload of the right side of the heart will cause an overload of the entire pulmonary vasculature.  Eventually the pulmonary vasculature will develop pulmonary hypertension to try to divert the extra blood volume away from the lungs.

The pulmonary hypertension will cause the right ventricle to face increased preload that the shunted blood from the left atrium to the right atrium caused.  The right ventricle will be forced to generate higher pressures to try to overcome the pulmonary hypertension.  This may lead to right ventricular failure (dilatation and decreased systolic function of the right ventricle) or elevations of the right sided pressures to levels greater than the left sided pressures.

When the pressure in the right atrium rises to the level in the left atrium, there will no longer be a pressure gradient between these heart chambers, and the left-to-right shunt will diminish or cease.

If left uncorrected, the pressure in the right side of the heart will be greater than the left side of the heart.  This will cause the pressure in the right atrium to be higher than the pressure in the left atrium.  This will reverse the pressure gradient across the ASD, and the shunt will reverse; a '''right-to-left shunt''' will exist.  This phenomenon is known as Eisenmenger's syndrome.

Once right-to-left shunting occurs, a portion of the oxygen-poor blood will get shunted to the left side of the heart and ejected to the peripheral vascular system.  This will cause signs of cyanosis.

==Epidemiology==
As a group, atrial septal defects are detected in 1 child per 1500 live births. PFO are quite common (appearing in 10 - 20% of adults) but asymptomatic and therefore undiagnosed. ASDs make up 30 to 40% of all congenital heart disease that is seen in adults.<!--
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The ostium secundum atrial septal defect accounts for 7% of all congenital heart lesions.  This lesion shows a female preponderance, with a male : female ratio of 1:2.<!--
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==Types of atrial septal defects==
right|thumb|350px|Schemating drawing showing the location of different types of ASD, the view is into an opened right atrium. ''HV'': right ventricle; ''VCS'': superior caval vein; ''VCI'': inferior caval vein; ''1'': upper sinus venosus defect; ''2'': lower sinus venosus defect; ''3'': secundum defect; ''4'': defect involving coronary sinus; ''5''; primum defect.
There are many types of atrial septal defects.  They are differentiated from each other by whether they involve other structures of the heart and how they are formed during the developmental process during early fetal development.

===Ostium secundum atrial septal defect===
The '''ostium secundum atrial septal defect''' is the most common type of atrial septal defect, and comprises 6-10% of all congenital heart diseases.

The secundum atrial septal defect usually arises from an enlarged foramen ovale, inadequate growth of the septum secundum, or excessive absorption of the septum primum.  10 to 20 percent of individuals with ostium secundum ASDs also have mitral valve prolapse .<!--
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====Natural history====
Most individuals with an uncorrected secundum ASD don't have significant symptoms through early adulthood.  About 70% develop symptoms by the time they are in their 40s.  Symptoms are typically decreased exercise tolerance, easy fatigueability, syncope.

Complications of an uncorrected secundum ASD include heart failure, flutter, stroke, and Eisenmenger's syndrome.

While pulmonary hypertension is unusual before 20 years of age, it is seen in 50% of individuals above the age of 40.  Progression to Eisenmenger's syndrome occurs in 5 to 10% of individuals late in the disease process.

====Patent foramen ovale====
A '''patent foramen ovale''' ('''PFO''') is a small channel that has little hemodynamic consequence; it is a remnant of the fetal foramen ovale. Clinically it is linked to decompression sickness, paradoxical embolism and migraine. On echocardiography, there may not be any shunting of blood noted except when the patient coughs.

There is debate within the neurology and cardiology communities about the role of a PFO in cryptogenic (ie of unknown cause) neurologic events, e.g. strokes and transient ischemia attacks (TIAs) without any other potential cause. In addition, there is some data to suggest that PFOs may be involved in the pathogenesis of some migraine headaches. Several clinical trials are currently underway to investigate the role of PFO in these clinical situations.

===Ostium primum atrial septal defect===
:
A defect in the ostium primum is occasionally classified as an atrial septal defect,<ref></ref>, but it is more commonly classified as an atrioventricular septal defect<ref name="isbn0-683-30272-8"></ref><ref></ref>

===Sinus venosus atrial septal defect===
A sinus venosus ASD is a type of atrial septum defect in which the defect in the septum involves the venous inflow of either the superior vena cava or the inferior vena cava.

A sinus venosus ASD that involves the superior vena cava makes up 2 to 3% of all interatrial communication.  It is located at the junction of the superior vena cava and the right atrium.  It is frequently associated with anomalous drainage of the right-sided pulmonary veins into the right atrium (instead of the normal drainage of the pulmonary veins into the left atrium).<!--
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right|thumb|250 px|[[Echocardiography|Ultrasound picture of the heart, seen in a subcostal view. The apex towards the right, atria to the left. ASD secundum seen as a discontinuation of the white band of the atrial septum. Enlarged right atrium below. Enlarged pulmonary veins seen entering left atrium above. (Echocardiogram: Wikipedia editor Kjetil Lenes (Ekko) )]]

===Common or single atrium===

Common (or single) atrium is a failure of development of the embryologic components that contribute to the atrial septal complex. It is frequently associated with heterotaxy syndrome <ref></ref>

==Diagnosis==
===Diagnosis in children===
Most individuals with a significant ASD are diagnosed in utero or in early childhood with the use of ultrasonography or auscultation of the heart sounds during physical examination.

===Diagnosis in adults===
Some individuals with an ASD will have undergone surgical correction of their ASD during childhood.  The development of signs and symptoms due to an ASD are related to the size of the intracardiac shunt. Individuals with a larger shunt tend to present with symptoms at a younger age.

Adults with an uncorrected ASD will present with symptoms of dyspnea on exertion (shortness of breath with minimal exercise), congestive heart failure, or cerebrovascular accident (stroke).  They may be noted on routine testing to have an abnormal chest x-ray or an abnormal EKG and may have atrial fibrillation.

====Physical exam auscultation of the heart====
The physical findings in an adult with an ASD include those related directly to the intracardiac shunt, and those that are secondary to the right heart failure that may be present in these individuals.

Upon auscultation of the heart sounds, there may be an ''ejection systolic murmur'' that is attributed to the pulmonic valve.  This is due to the increased flow of blood through the pulmonic valve rather than any structural abnormality of the valve leaflets.

Дефекты межпредсердной перегородки - это распространенный порок, чаще встречается у женщин. 

Дефекты межпредсердной перегородки типа sinus venosus располагаются в верхнем отделе межпредсердной перегородки, вблизи места впадения верхней полой вены, в этой же области часто обнаруживается и аномальное впадение правых легочных вен. 

Дефекты межпредсердной перегородки типа , напротив, располагаются в самом низу межпредсердной перегородки, над АВ-клапанами; последние часто изменены, возможны митральная недостаточность и трикуспидальная недостаточность. Дефекты межпредсердной перегородки типа ''ostium primum'' являются составной частью АВ-канала - порока, который особенно характерен для синдрома Дауна и может также включать дефекты АВ-перегородки и дефекты задненижнего отдела межжелудочковой перегородки и единый АВ-клапан (передняя створка митрального и перегородочная створка трехстворчатого клапанов соединены и образуют единую створку). 

Дефект межпредсердной перегородки типа ''ostium secundum'' - самый частый из дефектов межпредсердной перегородки - находится в ее центре, в области овальной ямки. Его надо отличать от открытого овального окна: вскоре после рождения оно обычно закрывается и зарастает (небольшое отверстие, пропускающее катетер, - вариант нормы). В случае же дефекта речь идет об отсутствии ткани межпредсердной перегородки, ведущем к сбросу крови. 