Congenital Left Ventricular Outpouching ( Lvo )

Atrioventricular Canal Defect is an abnormality that causes the mixing of blood. There is a hole in center of heart where the wall between the upper and lower chambers meet. The tricuspid and mitral valves aren’t formed properly and one large valve crosses the defect. The defect lets oxygen rich blood pass to the heart’s right side and mix with deoxygenated blood, then go back to the lungs. Another abnormality is Atrial Septal Defect (ASD), where the walls of the upper chambers of the heart don’t close completely, causing a left to right movement of blood due to the higher pressure. The mixing of oxygenated and deoxygenated blood may cause the right atrium and ventricle to enlarge due to the higher volume of blood.

The flow of blood through the heart is controlled by four valves. If any are not working correctly, blood cannot flow or be pumped effectively to the heart. The four valves are: the tricuspid, pulmonary semilunar, mitral, and aortic semilunar. There are many abnormalities or defects that can affect their operation and in this paper, I will discuss the most common one which is a “mitral valve prolapse.” A valvular prolapse is an abnormal protrusion of a heart valve that causes the valve to not close completely. It is also known as “click murmur syndrome” and “Barlow’s syndrome” and is more prevalent in women than men. It has a strong hereditary

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.

Tiffany is worried about her newborn son. Ever since she brought Caleb home from the hospital it has been so hard to get him to eat and he seems to be breathing too hard all the time. At his one month check-up, the nurse tells her that Caleb has only gained one pound since he was born and Tiffany breaks into tears.

Hypoplastic Left Heart Syndrome is a very serious birth defect. Studies say, “each year approximately… 640 to 1440 infants in the United States are born with HLHS” (Paediatr Child Health,2). Hypoplastic Left Heart Syndrome, also known as HLHS, is a birth defect where the left ventricle of the heart is either underdeveloped or absent. Today, there are heart surgeries that can help children born with HLHS survive longer and sometimes even live long, happy lives. Though, not all children survive HLHS. Many infants die whilst waiting for a donor heart.

A ventricular septal defect or VSD is a heart defect. It’s congenital, this means that a baby is born with it. It is an opening or hole in the dividing wall called the Septum, between the two lower chambers of the heart, right and left ventricles. Ventricular septal defects are the most common type of congenital heart defects. A VSD allows oxygen-rich blood to pass from the left ventricle through the opening in the septum. Then it mixes with oxygen-poor blood in the right ventricle. There are different types of ventricular septal defects, the type your child has depends on which part of the wall between the ventricles is involved. Also the size of the opening or hole varies. A ventricular septal defect may occur more often in some families, this is because of gene defects. But most of the time, the cause is unknown. Similarly to ventricular septal defect, an Atrial septal defect is a birth defect of the heart in which there is also a hole in the wall in the septum, but instead of dividing the lower chambers it divides the upper chambers of the heart (atria), here a hole can vary in size and may close on its own or may require surgery as well. An atrial septal defect is one type of congenital heart defect, in which also the baby is born with it.

One of the complications of an acute MI is Left Ventricular Aneurysm (LVA) which is a localized area of myocardium with abnormal outward bulging and deformation during systole and diastole. The epidemiology occurs in 10-30% of patients after an acute MI (American Heart Association 2015). The risk factors include total occlusion of the LAD artery, females and an anterior MI. To prevent this, early revascularization is needed. The LVAs usually range from 1-8 cm.

Haegeli, Laurent M., Ercüment Ercin, Jan Steffel, Thomas Wolber, Felix C. Tanner, Rolf Jenni, Oliver Gämperli, Ardan M. Saguner, Thomas F. Lüscher, Corinn Brunckhorst, and Firat Duru. " Incidence and Prognosis of Ventricular Arrhythmiasin Patients with Congenital Left Ventricular Aneurysms or Diverticula." The American Journal of Medicine 128.6 (2015): n. pag. Web.

One of the rarest of congenital cardiac defects is Hypoplastic Left Heart Syndrome, HLHS. This syndrome is described as a collection of anomalies affecting the left heart and connecting structures. Due to advancements in surgical intervention mortality rates in neonates with Hypoplastic Left Heart Syndrome have decreased. Management of these patients requires a symphony of multidisciplinary teams including fetal and pediatric cardiologist, cardiac surgeons, neonatologist, pulmonologist, nutritionist and family counselors. Options currently comprise of heart transplant, three-staged palliative surgery and comfort care. There may be co-morbidities present which further complicate treatment, but with surgical intervention the

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

HLHS is when the left side of the heart is severely underdeveloped. In hypoplastic left heart syndrome, the left side of the heart can 't properly supply blood to the body because the lower left chamber (left ventricle) is too small or in some cases it may not even exist. In addition, the valves on the left side of the heart (aortic valve and mitral valve) don 't work properly, and the main artery leaving the heart (aorta) is smaller than normal. The foramen ovale is a natural opening between the upper chambers of the heart (atria) or through a blood vessel that connects the pulmonary artery directly to the aorta (ductus arteriosus) and for the first several days of life, the right side of the heart can pump blood to both the lungs and the rest of the body through this. Often babies with HLHS undergo a three-staged set of complex surgeries in which the outcome is usually leaving the child with half a heart. In doing this, it increases the child’s chances of survival. The foramen ovale usually closes after the first day or two of life then the right side of the heart has no way to pump blood out to the body.

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

On ultrasound, there is a live fetus in breech presentation. Fetal biometry is symmetric and consistent with dates. A detailed anatomic survey was overall unremarkable but we were unable to adequately obtain fetal cardiac views in order to complete the echocardiogram. Both myself and the sonographer scanned and unfortunately the fetus remained in the spine up position after an extended amount of

Echocardiography is the initial diagnostic modality for a patient with suspected congenital heart disease. In some patients, however, use of this modality is encumbered by its limited ability to delineate great arteries and intra cardiac anomalies, pulmonary veins, and coronary arteries. (7)

Patent ductus arteriosus (PDA), one of the more common cardiac defects at birth, is the persistence of an opening between the pulmonary artery and the descending thoracic aorta. This opening is as a result of failure of the physiological fetus ductus arteriosus to close, which normally occurs soon after birth. This hole allows for oxygenated blood from the aorta to mix with oxygen-depleted blood from the pulmonary artery. As a consequence, significant strain is placed on the heart and pressure within the lungs’ arteries is dramatically increased.