• Ventricular Septal Defect (VSD)

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    A ventricular septal defect (VSD) is a hole in the wall that separates the heart’s left and right ventricles, the lower pumping chambers. The hole provides an opening for blood to cross the wall, or septum, from the left side to the right side of the heart. When this occurs, some of the blood in the left ventricle, which has just come back to the heart from picking up oxygen in the lungs, may go into the right ventricle and immediately back to the lungs. 

    These holes can exist in various parts of the wall between the bottom pumping chambers of the heart (septum): they can occur near the valves that let blood into the pumping chambers (inlet), the thick section of the septum (muscular), in the thinner fibrous area of the wall (perimembranous), toward the main vessel leaving the heart (outlet), or high up toward the valve that lets blood out to the lungs (supracristal).

    An increase in blood flow across the hole to the lungs can cause the lungs to become congested. Congestion of the lungs interferes with their job of transferring oxygen from the air to the blood and carbon dioxide from blood to air. The extra blood returning from the lungs to the left heart chambers can cause them to enlarge. When the heart is overburdened and the lungs become congested, a condition called congestive heart failure (CHF) occurs.

    Because the heart and lungs have to work harder, an infant with a VSD will become short of breath, particularly with the exertion of feeding (which is the most exercise an infant does). This could lead to poor feeding and eventually to poor weight gain and growth.

    Birth defects of the heart occur in 1 percent of all born children. Half of all patients with congenital heart disease have ventricular septal defects. Premature infants have a much higher incidence of ventricular septal defect: 10 times that of full-term babies. 


    If the VSD is small, the amount of increased blood flow into the lungs will not significantly increase and the child will not be noticeably affected. If it is larger and allows much more blood than normal to flow to the lungs, serious problems may result, including:  

    •  Fatigue of the heart, because it has to work harder to deal with the inefficient circulation of blood.
    •  Congestion of the lungs, leading to difficulty in breathing. 
    •  Poor weight gain because of an inability to tolerate the exertion needed to feed properly. 
    •  Decreased oxygen to the body if excessive damage has occurred to the lungs, causing difficulty in getting blood to pass through the lungs. In this case, the flow across the VSD may actually reverse, causing blue blood to go directly to the body (this is called Eisenmenger Syndrome).


    Some ventricular septal defects may spontaneously close without treatment, but the larger the defect, the less likely it is to do so. The location of the VSD in the ventricular septum also influences whether it closes on its own, with defects in the thicker muscular part of the septum being the most likely to close over time.

    If a moderate or large VSD is not treated, the result may be irreversible damage to the blood vessels of the lungs and can even cause blood flow to reverse so blue blood goes directly to the body (Eisenmenger Syndrome). Patients with Eisenmenger Syndrome are more likely to suffer from strokes and brain infections. If the damage progresses, death can result, typically in the fourth or fifth decade of life. 


    Some VSDs, particularly muscular and perimembranous ones, may close by themselves over time and cardiologists may wait to see if this happens. However, surgery is often necessary if there is too much blood passing through the holes or if there is increasing leakage found of the aortic valve over time. Some VSDs can be successfully closed in the hospital’s catheterization lab using special devices, thus avoiding open-heart surgery.


    If the VSD does not close on its own, the cardiologist may recommend anti-congestive heart failure medications. These may include:

    • Diuretics: The most commonly prescribed diuretics are furosemide (Lasix) and thiazides (Diuril and Hydrodiuril). Diuretics act to cause the child to pass more urine, leading to a smaller blood volume – and a smaller burden on the heart to pump. Another commonly used diuretic is spiranolactone (Aldactone). It has a weak diuretic effect and is mainly used because it helps the kidneys retain potassium. Other diuretics tend to waste potassium excessively.  
    • Inotropes: These medications, which include digoxin, help the heart pump more efficiently (stronger while using less energy). 
    • Afterload-reducing agents: These drugs, which include captopril, are sometimes used in the treatment of VSD. However, when used, they act to help blood flow to the body and perhaps less to the lungs. This leads to less blood crossing the ventricular septal defect – and reduction in congestive heart failure. 

    Surgical Closure of VSD

    Open-heart surgery may be recommended if the VSD is too large, medications are not helping, if the function of the valves is affected, or if the child is beyond an age when the VSD may close by itself. During surgery, the surgeon opens the heart and closes the defect by using a patch or sutures. The child who undergoes surgery may stay in the hospital three to five days.

    Occasionally, surgery may be recommended if the VSD is not large but is causing damage to the nearby aortic valve, the structure that keeps blood flowing out in one direction from the heart’s left ventricle to the aorta, the vessel that carries blood from the heart to the rest of the body. This may cause the valve to leak due to distortion of the valve leaflets.