Common Prenatal Congenital Heart Disease Essay

Congenital heart disease is a cardiovascular condition resulting from an abnormality in the structure of the heart. The exact time this defect forms is unknown but it is during the fetal development in the womb. Researchers think the defect could be case partially by genetics and medical conditions of the fetus and the parents. If the baby’s mother had rubella, while pregnant or other conditions such as diabetes could have caused the defect. Some medications that were taken by a pregnant mother could also have caused birth defects. An error on chromosome 22 could also have caused the heart defect. Some symptoms that a person may have a congenital heart may not show up until later in life but many children also have the symptoms. Symptoms of a congenital heart defect are abnormal heartbeat, bluish tint to skin, shortness of breath, dizziness or fainting, and swelling of body tissues and organs.

The blood that does not cross the foramen ovale into the left atrium is emptied into the right ventricle which is then pumped into the pulmonary artery to be carried to the lungs. The third fetal shunt is encountered; the ductus arteriosus allows blood to be shunted from the pulmonary artery to the aorta and systemic arteries following. Blood that does go to the lungs are returned by the pulmonary veins to the left atrium and emptied into the left ventricle. (Perinatal and Pediatric Respiratory Care, Ch2 p 17-18) Shortly after birth due to changes in vascular resistance blood is redirected to the lungs for oxygenation and these shunts are no longer required leading to their closure within a few days postpartum. In HLHS, because the left heart structures are insufficient to receive and pump adequate amounts of oxygenated blood to supply the tissues the patency of the foramen ovale and the ductus arteriosus are essential to sustaining life. (PubMed – ADAM Medical Encyclopedia, 2013) Medical intervention is needed to maintain the patency of the ductus arteriosus and an atrial septal defect is created in place of the foramen ovale.

Tetralogy of Fallot (ToF) is a rare, complex congenital heart defect. It occurs in about five out of every 10,000 babies. When babies are born with ToF, they have four different heart problems:

Critical Congenital Heart Defect (CCHD) is a subgroup of congenital heart defects that normally necessitates surgical intervention or catheterization procedure during the neonatal period (Good, Canale, Goodman, & Yeager, 2015). According to Mahle et al. (2009), although there are measures taken to detect CCHD like prenatal ultrasound and comprehensive newborn physical examination during newborn’s birth hospitalization, there is still a significant percentage of newborns with CCHD that is left undetected and discharged home without being diagnosed. Delay in diagnosis of CCHD increases morbidity and mortality (Mahle et al., 2009). In response to this, Riede et al. (2010) mentioned that the diagnostic gap in CCHD could be bridged by screening newborns using pulse oximetry

Views today demonstrate a viable singleton fetus at 12 weeks 2 days. Fetal crown-rump length measures 59.2 mm. The best nuchal translucency measurement obtained was 1.8 mm, and the nasal bone was visualized as present. Fetal cardiac activity is visualized. Due to early gestational age, fetal anatomy was not assessed, but 4 extremities are noted. Amniotic fluid and placental location are visualized as normal within limitations of early gestational age. Adnexa are suboptimally seen. No notching is seen on the uterine artery Doppler’s.

On today’s evaluation, she is 19 weeks and the fetal measurements overall are concordant. The long bone measurements are within one week of her dates. The amniotic fluid volume is normal, and the cervix is long and closed. A complete fetal anatomical survey was performed and a significant amount of ventriculomegaly/hydrocephalous was identified but no other major malformations were noted at this time, though due to the

The incidence of PDA is approximately 0.02 to 0.04 percent in term infants and 20 to 60 percent in preterm neonates. Patent ductus arteriosus accounts for six to eleven percent of all congenital heart defects. PDA is found twice as often in females than in males (Shinde, Basantwani, & Tendolkar, 2016). The incidence of PDA is increased in children who are born prematurely, children with a history of perinatal asphyxia, and, possibly, children born at high altitude. Up to 30 percent low birth infants develop PDA (Kim, 2016).

The heart cannot help but break for the suffering of children who are marked by the cruelty of congenital diseases. One such disease is tetralogy of tallot which as a congenital ailment occurs at birth and involves four different kinds of cardial defects (Mayo Clinic, 2015). The incidents of tetralogy of fallot is actually quite rare with only five out of every 10,000 developing it at birth (National Heart, Lung, and Blood Institute, 2011). It is still important to be familiar with. One reason for the need of understanding the disease is that of all congenital heart disorders it is the one most frequently seen, and the mortality rate is another consideration as 50% will not survive past the age of six should tetralogy of fallot be left untreated (Bhimji & Mancini, 2015). Finally, while vast improvements have been made in intervention of the disease improving survivability the condition will have an effect upon a patients throughout their lifetimes. It is because of these that it is important for early recognition, diagnosis, treatment and care of the disease be enacted to ensure not only a positive health outcome but also a good quality of life.

Medical studies report that there is no known cause of TOF. There is some things that can be seen in TOF babies but not the diffident cause. Such as, low oxygen levels, narrowing of the pulmonary outflow tract, thickened wall of the right ventricle and a VSD. However, there are a few genetic syndromes that have been reported. Such as, Down syndrome or DiGeorge syndrome (UMMC, 2013). To add to that, most people with TOF do not have genetic syndromes. Tetralogy Of Fallot does not typically run in families. Although, congenital heart defects are to some extent more common if there is a close relative who has one.

Isolated case reports, however, provide the only information about the evolution in the uterus of this spectrum of diseases in the second and third trimesters, and they suggest potential progression in the degree of left heart hypoplasia. Therefore, in the present study, the researchers retrospectively reviewed the prenatal and postnatal echocardiograms of 21 fetuses with left heart obstructive lesions. Table 1 shows the research that was found on the 21 fetuses (Hornberger et al; 1995). The researcher also attempted to identify prenatal features that could indicate the severity of postnatal left heart obstruction and hypoplasia. Fetuses were divided into groups according to whether postnatally the left heart was capable or incapable of supporting the systemic circulation in the presence of a patent aortic valve. Group 3 included fetuses with aortic atresia. At the initial examination, left heart dimensions were normal or reduced, with the most unusually small measurements in group 3. Three fetuses in group 2 and most in group 1 had normal initial left heart dimensions. Subsequent growth of left heart structures either paralleled normal growth or was reduced, the latter resulting in the development or progression of left heart hypoplasia. All left heart dimensions grew more slowly in group 2 and group 3 than in group 1. Other prenatal features observed only in groups 2 and 3 included reversed or bidirectional foramen ovale flow and retrograde distal arch flow. Initial mid-trimester mitral valve and the growth rates of all left heart structures correlated strongly with postnatal left ventricular end-diastolic dimension, there could be additional indicators of postnatal disease severity. In group 1, one fetus developed severe aortic stenosis late in

Tetralogy of Fallot (TOF) is a congenital heart defect that presenting at birth. It represents about 10% of cases of congenital heart defect, it occurs in 3 to 6 infants per 10,000 births.

Cyanotic congenital heart defects include; Transposition of the great arteries, Truncus arteriosus, Total anomalous pulmonary venous connection. (5)

A family is grieving. Their five years daughter has already undergone one open-heart surgery for a serious congenital heart disease. Then, the doctor told her parents that the girl needed a transplant. The five year old girl could not walk or eat and finally, she is put in intensive care (Pathos). This sounds all too real right. Well, it is. This is the tale of a Chinese girl, Shutong. Luckily, in October 2000, she received the heart of donor Matthew, a four-year-old typical boy who liked playing with cars and watching movies. However, his gift of life was far from typical (Life Stories: A New Heart Helps a Young Girl…). This story had a happy ending but so many do not.

It is the time of progress. The time of supercomputers, space shuttles, and many other wonders of technology. We have walked on the moon. We do our shopping at home via Internet navigation.

From the very first time the heart starts pounding until the time of death, it may beat more than 3.5 billion times. The center of the circulatory system is the heart. The average heart beats 100,000 times each day, pushing around 2,000 gallons of blood throughout your body. With a life span of 70-90, the heart will beat two to three billion times and circulate 50-65 million gallons of blood.