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If the defect involves two or more of the septal zones, then the defect is termed a mixed atrial septal defect.
In unaffected individuals, the chambers of the left side of the heart are under higher pressure than the chambers of the right side because the left ventricle has to produce enough pressure to pump blood throughout the entire body, while the right ventricle needs only to produce enough pressure to pump blood to the lungs.
This extra blood from the left atrium may cause a volume overload of both the right atrium and the right ventricle. If untreated, this condition 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 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 left-to-right shunt increases the filling pressure of the right heart preload and forces the right ventricle to pump out more blood than the left ventricle.
This constant overloading of the right side of the heart causes an overload of the entire pulmonary vasculature. Eventually, pulmonary hypertension may develop.
The pulmonary hypertension will cause the right ventricle to face increased afterload. The right ventricle is 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. If the ASD is left uncorrected, the pulmonary hypertension progresses and the pressure in the right side of the heart becomes greater than the left side of the heart.
This reversal of the pressure gradient across the ASD causes the shunt to reverse - a right-to-left shunt. This phenomenon is known as Eisenmenger's syndrome.
Once right-to-left shunting occurs, a portion of the oxygen-poor blood gets shunted to the left side of the heart and ejected to the peripheral vascular system.
This causes signs of cyanosis. 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.
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 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 ECG and may have atrial fibrillation. If the ASD causes a left-to-right shunt, the pulmonary vasculature in both lungs may appear dilated on chest X-ray, due to the increase in pulmonary blood flow.
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 , a systolic ejection murmur may be heard that is attributed to the pulmonic valve, due to the increased flow of blood through the pulmonic valve rather than any structural abnormality of the valve leaflets.
In unaffected individuals, respiratory variations occur in the splitting of the second heart sound S 2. During respiratory inspiration, the negative intrathoracic pressure causes increased blood return into the right side of the heart.
The increased blood volume in the right ventricle causes the pulmonic valve to stay open longer during ventricular systole.
This causes a normal delay in the P 2 component of S 2. During expiration, the positive intrathoracic pressure causes decreased blood return to the right side of the heart.
The reduced volume in the right ventricle allows the pulmonic valve to close earlier at the end of ventricular systole, causing P 2 to occur earlier.
In individuals with an ASD, a fixed splitting of S 2 occurs because the extra blood return during inspiration gets equalized between the left and right atria due to the communication that exists between the atria in individuals with ASD.
The right ventricle can be thought of as continuously overloaded because of the left-to-right shunt, producing a widely split S2.
Because the atria are linked via the atrial septal defect, inspiration produces no net pressure change between them, and has no effect on the splitting of S2.
In transthoracic echocardiography , an atrial septal defect may be seen on color flow imaging as a jet of blood from the left atrium to the right atrium.
If agitated saline is injected into a peripheral vein during echocardiography, small air bubbles can be seen on echocardiographic imaging.
Bubbles traveling across an ASD may be seen either at rest or during a cough. Bubbles only flow from right atrium to left atrium if the right atrial pressure is greater than left atrial.
Because better visualization of the atria is achieved with transesophageal echocardiography, this test may be performed in individuals with a suspected ASD which is not visualized on transthoracic imaging.
Newer techniques to visualize these defects involve intracardiac imaging with special catheters typically placed in the venous system and advanced to the level of the heart.
This type of imaging is becoming more common and involves only mild sedation for the patient typically. If the individual has adequate echocardiographic windows, use of the echocardiogram to measure the cardiac output of the left ventricle and the right ventricle independently is possible.
In this way, the shunt fraction can be estimated using echocardiography. The ECG findings in atrial septal defect vary with the type of defect the individual has.
Individuals with atrial septal defects may have a prolonged PR interval a first-degree heart block. The prolongation of the PR interval is probably due to the enlargement of the atria common in ASDs and the increased distance due to the defect itself.
Both of these can cause an increased distance of internodal conduction from the SA node to the AV node. A common finding in the ECG is the presence of incomplete right bundle branch block , which is so characteristic that if it is absent, the diagnosis of ASD should be reconsidered.
ASD with pulmonary embolism resulting in a right to left shunting of blood . Most patients with a PFO are asymptomatic and do not require any specific treatment.
In those where a comprehensive evaluation is performed and an obvious etiology is not identified, they are defined as having a cryptogenic stroke.
The mechanism for stroke is such individuals is likely embolic due to paradoxical emboli, a left atrial appendage clot, a clot on the inter-atrial septum, or within the PFO tunnel.
Until recently, patients with PFO and cryptogenic stroke were treated with antiplatelet therapy only. Previous studies did not identify a clear benefit of PFO closure over antiplatelet therapy in reducing recurrent ischemic stroke.
However, based on new evidence    and systematic review in the field,  percutaneous PFO closure in addition to antiplatelet therapy is suggested for all who meet all the following criteria: A variety of PFO closure devices may be implanted via catheter-based procedures.
Based on the most up to date evidence, PFO closure is more effective at reducing recurrent ischemic stroke when compared to medical therapy.
In most of these studies, antiplatelet and anticoagulation were combined in the medical therapy arm. Although there is limited data on the effectiveness of anticoagulation in reducing stroke in this population, it is hypothesized that based on the embolic mechanism, that anticoagulation should be superior to antiplatelet therapy at reducing risk of recurrent stroke.
A recent review of the literature supports this hypothesis recommending anticoagulation over the use of antiplatelet therapy in patients with PFO and cryptogenic stroke.
Once someone is found to have an atrial septal defect, a determination of whether it should be corrected is typically made.
If the atrial septal defect is causing the right ventricle to enlarge a secundum atrial septal defect should generally be closed.
Prior to correction of an ASD, an evaluation is made of the severity of the individual's pulmonary hypertension if present at all and whether it is reversible closure of an ASD may be recommended for prevention purposes, to avoid such a complication in the first place.
Pulmonary hypertension is not always present in adults who are diagnosed with an ASD in adulthood. If pulmonary hypertension is present, the evaluation may include a right heart catheterization.
This involves placing a catheter in the venous system of the heart and measuring pressures and oxygen saturations in the superior vena cava, inferior vena cava, right atrium, right ventricle, and pulmonary artery, and in the wedge position.
Individuals with a pulmonary vascular resistance PVR less than 7 wood units show regression of symptoms including NYHA functional class.
However, individuals with a PVR greater than 15 wood units have increased mortality associated with closure of the ASD.
If the pulmonary arterial pressure is more than two-thirds of the systemic systolic pressure, a net left-to-right shunt should occur at least 1.
If Eisenmenger's physiology has set in, the right-to-left shunt must be shown to be reversible with pulmonary artery vasodilators prior to surgery.
Surgical mortality due to closure of an ASD is lowest when the procedure is performed prior to the development of significant pulmonary hypertension.
The lowest mortality rates are achieved in individuals with a pulmonary artery systolic pressure less than 40 mmHg. If Eisenmenger's syndrome has occurred, a significant risk of mortality exists regardless of the method of closure of the ASD.
In individuals who have developed Eisenmenger's syndrome, the pressure in the right ventricle has raised high enough to reverse the shunt in the atria.
If the ASD is then closed, the afterload that the right ventricle has to act against has suddenly increased. This may cause immediate right ventricular failure, since it may not be able to pump the blood against the pulmonary hypertension.
Surgical closure of an ASD involves opening up at least one atrium and closing the defect with a patch under direct visualization.
Percutaneous device closure involves the passage of a catheter into the heart through the femoral vein guided by fluoroscopy and echocardiography.
The catheter is placed in the right femoral vein and guided into the right atrium. The catheter is guided through the atrial septal wall and one disc left atrial is opened and pulled into place.
Once this occurs, the other disc right atrial is opened in place and the device is inserted into the septal wall. This type of PFO closure is more effective than drug or other medical therapies for decreasing the risk of future thromboembolism.
Percutaneous closure of an ASD is currently only indicated for the closure of secundum ASDs with a sufficient rim of tissue around the septal defect so that the closure device does not impinge upon the superior vena cava, inferior vena cava, or the tricuspid or mitral valves.
The ASO consists of two self-expandable round discs connected to each other with a 4-mm waist, made up of 0. Implantation of the device is relatively easy.
The prevalence of residual defect is low. The disadvantages are a thick profile of the device and concern related to a large amount of nitinol a nickel-titanium compound in the device and consequent potential for nickel toxicity.
Percutaneous closure is the method of choice in most centres. As a group, atrial septal defects are detected in one child per live births.
This lesion shows a male: From Wikipedia, the free encyclopedia. A heart defect present at birth in which blood can flow through an opening between the top chambers of the heart.
Ostium primum atrial septal defect. Heart of human embryo of about 35 days. Diagnosing ASD can be difficult since there is no medical test, like a blood test, to diagnose the disorders.
ASD can sometimes be detected at 18 months or younger. By age 2, a diagnosis by an experienced professional can be considered very reliable. This delay means that children with ASD might not get the early help they need.
There is currently no cure for ASD. Services can include therapy to help the child talk, walk, and interact with others.
Even if your child has not been diagnosed with an ASD, he or she may be eligible for early intervention treatment services. The Individuals with Disabilities Education Act IDEA says that children under the age of 3 years 36 months who are at risk of having developmental delays may be eligible for services.
These services are provided through an early intervention system in your state. Through this system, you can ask for an evaluation. In addition, treatment for particular symptoms, such as speech therapy for language delays, often does not need to wait for a formal ASD diagnosis.
We do not know all of the causes of ASD. However, we have learned that there are likely many causes for multiple types of ASD.
There may be many different factors that make a child more likely to have an ASD, including environmental, biologic and genetic factors. ASD continues to be an important public health concern.
Understanding the factors that make a person more likely to develop ASD will help us learn more about the causes. We are currently working on one of the largest U.
SEED is looking at many possible risk factors for ASD, including genetic, environmental, pregnancy, and behavioral factors. ASD occurs in all racial, ethnic, and socioeconomic groups, but is about 4 times more common among boys than among girls.