“Definition”

Atrial septal defect (ASD) is a form of congenital heart defect that enables blood flow between the left
and right atria via the interatrial septum. The interatrial septum is the tissue that divides
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.[1]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 right side of the heart contains venous blood with a low oxygen content, and the left side of the heart
contains 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 improperly.

During development of the fetus, the interatrial septum develops to eventually separate
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).

“Cause”

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 ventricleonly 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 valveduring 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 hypertensionto try to divert
the extra blood volume away from the lungs.

The pulmonary hypertension will cause the right ventricle to face increased afterload in addition to the
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; aright-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.

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.[2]

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.[3]

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.