My Motivation

I think some people might wonder why I am getting so involved in raising awareness about CHD. After all, my son is recovering well and there's no reason to think he will ever need any further cardiac intervention. I do this for Drew, yes, and for my future children and grandchildren, of course. But I do this for the countless numbers of children who will never see their first birthdays, never graduate from high school, never hold their own precious baby in their arms. I do this for the countless numbers of parents who have to bury their sweet angels and figure out how to go on with life after such unimaginable heartache. I do this for everyone I will never meet and for all those I have been blessed to meet along this journey, and will be blessed to meet in the weeks, months, and years to come. And today, I am especially dedicated to the cause because of a CHD angel called Aiden. Aiden fought with tremendous courage in the face of mounting obstacles to come back to his Mommy and Daddy...and unfortunately, it was too much for his little body and he lost his battle. With his Mommy holding him closely to her, he went home to be with God on April 17th.

Educational Tidbit...here are the CHDs that Aiden had:

Pulmonary atresia (PA) is a complicated congenital (present at birth) defect that occurs when the pulmonary valve, located between the right ventricle and pulmonary artery, is not formed properly. The pulmonary valve has three leaflets that function like a one-way door, allowing blood to flow forward into the pulmonary artery, but not backward into the right ventricle. With pulmonary atresia, problems with valve development prevent the leaflets from opening, therefore, blood cannot flow forward from the right ventricle to the lungs. Before birth, while the fetus is developing, this is not a threat to life, because the placenta provides oxygen for the baby, and the lungs are not functional. Blood entering the right side of the fetal heart passes through an opening called the foramen ovale, which allows oxygen-rich (red) blood to pass through to the left side of the heart and proceed to the body. In some cases, there may be a second opening, this time in the ventricular wall, that allows blood in the right ventricle a way out. This opening is called a ventricular septal defect (VSD). If there is no VSD, the right ventricle receives little blood flow before birth and does not develop fully. After birth, the placenta no longer provides oxygen for the newborn, the lungs must provide it. With no pulmonary valve opening present, however, blood must find another route to reach the lungs and receive oxygen. The foramen ovale normally shuts at birth, but may stay open in this situation, allowing oxygen-poor (blue) blood to pass from the right atrium to the left atrium. From there, it goes to the left ventricle, out the aorta, to the body. This situation cannot support life, since oxygen-poor (blue) blood cannot meet the body's demands. Newborns also have a connection between the aorta and the pulmonary artery, called the ductus arteriosus, that allows some of the oxygen-poor (blue) blood to pass into the lungs. Unfortunately, this ductus arteriosus normally closes within a few hours or days after birth. Because of the low amount of oxygen provided to the body, pulmonary atresia is a heart problem that is labeled "blue-baby syndrome." Pulmonary atresia occurs in about one out of every 10,000 live births. Pulmonary atresia occurs due to the improper development of the heart during the first eight weeks of fetal growth. Some congenital heart defects may have a genetic link, either occurring due to a defect in a gene, a chromosome abnormality or environmental exposure, causing heart problems to occur more often in certain families. Most of the time, this heart defect occurs sporadically (by chance), with no clear reason for its development.

Tetralogy of Fallot occurs when the right side of the heart does not develop properly while a baby is in the mother's womb. A French physician, Etienne Fallot first described it, in 1888. The cause of the problem is not understood. The parts of the heart affected are the pulmonary valve, right ventricle and the ventricular septum. It is the most common form of cyanotic congenital heart disease and is slightly more common in males. It affects one out of every 1000 babies born with congenital heart disease. This heart problem is known to be associated with other congenital problems including Goldenhar syndrome, velo-cardio-facial syndrome, and DiGeorge syndrome. In tetralogy of Fallot, the area of the right ventricle that leads to the pulmonary artery is narrow . In addition, the pulmonary valve itself is often small causing further obstruction of blood flow to the lungs. These areas of narrowing make the right ventricle work harder to get blood past the blockage and results in thickening of the muscle of the right ventricle. This thickening of the muscle is called right ventricular hypertrophy. Another part of this heart defect is a hole in the wall of the heart (called the septum) that separates the right and left ventricle. This hole, called a ventricular septal defect, allows blue blood from the thick, narrow, high-pressure right ventricle to cross over to the lower pressure left ventricle where it mixes with red blood. The mixing of red blood with blue blood before the blood is sent out to the body is what causes the baby to appear blue. This blue color which is seen in the lips and under the fingernails is called cyanosis. The degree of cyanosis is dependent on the severity of the narrowing in the right ventricle. The fourth part of the defect as originally described by Dr. Fallot is the altered position of the aorta called aortic override.

Both are extremely serious conditions. I fight on in his name.