Q.

How does atrial septal defect cause hypertension?

Asked by KAVITA MISHRA ·

Medically reviewed by SecondMedic medical review team

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Answered by SecondMedic Expert

Cardiologist · Cardiology / Heart disease

Atrial septal defect (ASD) is a congenital heart defect that occurs when a hole forms in the wall that separates the two upper chambers of the heart, known as the right and left atria. This type of heart defect can cause an increase in blood pressure due to increased blood flow between those chambers. When too much blood flows through this opening, it can increase pressure on the pulmonary arteries and veins, leading to problems like pulmonary hypertension or high blood pressure in your lungs.

The most common way ASD causes hypertension is by increasing resistance to venous return back to your heart from other parts of your body, especially from your lower extremities. In turn, this causes increased preload (the amount of ventricular filling during diastole), which results in increased afterload—the amount of force opposing ejection outflow from each ventricle during systole—and therefore increases cardiac output and systemic arterial pressures. Since most people with ASD also have congestive heart failure due to poor cardiac function caused by valve defects or enlargement of certain structures within their hearts, they tend to be more prone than healthy individuals to having elevated systemic arterial pressures secondary to decreased compliance in their smaller vessels because fluid builds up more quickly around them as well.

In addition, some people with ASD also experience episodes called "arrests" whereby their hearts suddenly stop pumping completely for several seconds due to abnormal electrical activity within them; these arrests are associated with significant rises in systemic arterial pressure levels due only momentarily before returning back down normal ranges shortly afterwards. Lastly, calcified deposits can form around holes present within the interatrial septa found on patients with ASD; these calcified deposits are known as atheromatous plaques and they further reinforce already-existing resistances present along larger vessels leading away from affected areas such that even relatively small deficits within one’s circulatory system (such as those caused by ASDs) become amplified under relevant physiological conditions thus causing elevations in both local vascular tone and overall systemic pressures far greater than one would expect otherwise without such lesions existing alongside them inside our bodies.

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