Patent Ductus Arteriosus

Ventricular septal defect cause the blood flow move from high pressure, left ventricle, into the right ventricle, which has lower pressure. Oxygenated blood instead of going to the systemic circulation enters into the left ventricle and goes into the pulmonary artery and to the lungs. As the result return of the blood from the lungs to the left atrium and eventually into the left ventricle, will increase and cause dilation and hypertrophy of the chambers, increases end-diastolic pressure, and raise the pulmonary venous pressure. By increasing the pulmonary blood flow, the pulmonary capillary pressure also rises and that can increase the interstitial fluid in the lungs, and cause pulmonary edema. Finally, as blood goes through the gap, from the LV to the RV, away from the aorta, case the cardiac output to drop,

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.

2. The defect in Caleb’s heart allows blood to mix between the two ventricular chambers. Due to this defect would you expect the blood to move from left-to-right ventricle or right-to-left ventricle during systole? Explain your answer based on blood pressure and resistance in the heart and great vessels. It goes left to right during systole. The difference is normally, oxygen-poor (blue) blood returns to the right atrium from the body, travels to the right ventricle, and then is pumped into the lungs where it receives oxygen. Oxygen-rich (red) blood returns to the left atrium from the lungs, passes into the left ventricle, and then is pumped out to the body through the aorta. But when an infant has ventricular septal defect it still allows oxygen-rich (red) blood to pass from the left ventricle, through the opening in the septum, and then mix with oxygen-poor (blue) blood in the right ventricle. (ROCHESTER.EDU) but instead when systole occurs the blood gets mixed because of the septum therefore heart needs to pump harder to ensure that enough blood with oxygen reaches the body.

AS can occur in the congenital period or later in life, but is more common in adults due to lack of exercise, and nutrition causing calcium buildup. If it is congenital it will occur within the first eight weeks of pregnancy, which the cause is unknown. In a child with AS, the pressure is much higher than normal in the left chamber pumping. Blood that has leaked back into the left ventricle through the valve in between heartbeats, causing the ventricle to be enlarged. There are three stages of AS. Stage A occurs in patients with bicuspid aortic valve or aortic sclerosis who are symptom free but are at risk for AS. In stage B people have progressive AS with mild or moderate calcify valve leaflets, leaflets mobility, or mild or

Syndrome. Approximately half of all infants born with Down’s syndrome have a heart defect. Many of these defects have serious implications”

For both Atrial and Ventricular septal defect the size of the opening or hole affects how severe the child’s

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

Tetrology of Fallot(TOF) is the most common prenatal congenital cyanotic heart disease accounts for about 1/3600 live births and about 7% to 10% of of all congenital heart disease and is the most common cause of cyanosis in the neonatal period1 , 2. Typical Tetralogy of Fallot (TOF) may be missed in Four chamber view. An abnormal Four chamber view is rarely seen in typical TOF cases . In the typical form of TOF the fetal echocardiography is often characterized by a normal four-chamber view, a subaortic Ventricular septal defect (VSD), Dilated over riding of aorta seen in a LVOT view, Pulmonary stenosis and an increased Aorta/Pulmonary artery ratio, minimal antegrade flow in the main pulmonary artery and the aortic flow originated from right and left ventricle. All pregnant women with low risk factors , suspected fetal cardiac anomalies and with increased risk factors should be analyzed by extended fetal echo during the level 2 scan (18 – 22 weeks scan ). It is also important to identify the side of the aortic arch, which is quite easier in the prenatal period in three vessel view . This will be useful if surgery is planned postnatally. Extracardiac abnormalities, such as midline defects, central nervous system and renal abnormalities may be found in fetuses with TOF. These extracardiac defects are associated with chromosomal abnormalities. When TOF is diagnosed, serial follow up scans at 5 – 6 weeks intervals are adviced to know about the growth of the

The S-A node signal is delayed by the atrioventricular node to allow the full contraction of the atria that allows the ventricles to reach their maximum volume. A sweeping right to left wave of ventricular contraction then pumps blood into the pulmonary and systemic circulatory systems. The semilunar valves that separate the right ventricle from the pulmonary artery and the left ventricle from the aorta open shortly after the ventricles begin to contract. The opening of the semilunar valves ends a brief period of isometric (constant volume) ventricular contraction and initiates a period of rapid ventricular ejection.

Owen is a 2 month old male with the above mentioned cardiac history. He was brought to our clinic for first visit after being discharged from PICU. His bilateral PAs stenosis improved significantly after having PA branches balloon angioplasty and LPA stenting 6/6/2017. His echo today showed max pressure gradient of 23 mmHg across the LPA stent and 17 at the distal RPA and RVH with mild dynamic RVOTO when he bears down. In addition, he had moderate pulmonary valve regurgitation with minimal gradient across his RV-PA conduit. In the future, Owen will likely require further intervening on the narrowed LPA and RPA as well as on his RV-PA conduit. Timing to be detirmend by his longitudinal follow up. In term of PACs, it is currently well-controlled

Congenital heart diseases (CHDs) are the most prevalent of all birth defects and the leading cause of death in the first year of life, (1) with an annual prevalence ranging from six to twelve affected infants per 1,000 live births. (2)

Other defects or anomalies can greatly affect the pathophysiology such as coarctation of the aorta with ventricular septal defect, which is a defect in the septal wall causing the heart to have to work even harder. Another common anomaly is coarctation of the aorta with patent ductus arteriosus, which is a hole in the aorta causing the blood to skip a necessary step for circulation. The more cardiac defects the patient has the more complications the patient will incur and creating a more difficult or risky medical and/or surgical intervention, or long term affects that may require medications, or additional surgeries later in life.

One symptom is heart murmur. Heart murmur is when your heart makes swishing sound heard in you heart. Other symptoms that are typically known is shortness of breath. This can happen when exercising or doing some kind of body workout. These treatment can be treated by different kinds of things. This disorder can be treated by doing heart surgery or cardiac catheterization. For the surgery they will stitch up the hole with surgical materials or your body’s own tissue. Cardiac catheterization is when they put a flexible tube in your heart to insert a device in the hole to cover it. People who have atrial septal defect face fewer challenges in their daily

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.