A 7 month old male infant was born with a Double Outlet Right Ventricle. He underwent surgery one day after he was born. He had a BT [Blalock-Taussig] shunt placed to help with movement of the blood throughout his body and decrease the resistance on the pulmonary arteries. He was sent home five days after that surgery in May. Then on September 29th he was brought to Morton Meese Plant Hospital with dyspnea and in severe respiratory distress.
He was transferred to All Children’s hospital that day. At the point he arrived at all children’s hospital he was very sick. He was intubated with nitric oxide inhaled through the ventilator. It was found that this was not working for him they placed him on Extracorporeal membrane oxygenation
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Then work on getting him his surgery to fix his heart. He has already had two surgeries. He is at this time; he is awake most of the time and we should be looking to him getting off the ventilator soon.
It is explained more on how much the baby has to go to get better from their heart defect. It really depends on the severity and how complicated the surgery is to fix the defect. It is said that most children go through one surgery after it is found then when they get to a certain age or size the defect will be fixed permanently. It sometimes goes by a case by case basis. If they are treated and keep up with the treatment when they are waiting for the final surgery they will be fine.
Double outlet right ventricle (DORV) is a rare congenital heart defect (the baby is born with it) involving the "great arteries" (the aorta and the pulmonary artery). In a normal heart, the aorta exits from the left ventricle and pumps blood to the body, while the pulmonary artery exits from the right ventricle and pumps blood to the lungs (where it picks up oxygen). In DORV, the aorta and the pulmonary artery both come out of the right ventricle [Cleveland, 2011]. The cause is really not known. This is also a cyanotic heart defect. The baby will have a grey or blue appearance in the lips and fingers. The symptoms are a heart murmur, breathing problems, SOB, rapid breathing, difficulty eating or
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.
One of the most common surgeries performed on babies is called Esophageal Atresia/Tracheoesophageal Fistula. That is just the medical term for when a baby is born with a defect in their esophagus and trachea and needs to have it repaired. About 90% of babies are born with this condition. It occurs in 1 in 3,000 to 5,000 newborns. The good thing is that since it happens so frequently, the survival rate is almost 100%. The most rarest condition is ectopia cordis. That is when a baby is born with their heart outside of their chest. Ectopia Cordis occurs 8 per one million live births. The survival rate is very low. 90% of the babies are either stillborn or pass away within the first week of being out of the womb.
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.
In a normal human being the heart correctly functions by the blood first entering through the right atrium from the superior and inferior vena cava. This blood flow continues through the right atrioventricular valve into the right ventricle. The right ventricle contracts forcing the pulmonary valve to open leading blood flow through the pulmonary valve and into the pulmonary trunk. Blood is then distributed from the right and left pulmonary arteries to the lungs, where carbon dioxide is unloaded and oxygen is loaded into the blood. The blood is returned from the lungs to the left
He was non-verbal and non-ambulatory, spastic quadriplegic and hydrocephalic. He had a history of asthma, and respiratory distress. Due to congenital malformation of his head, neck and trachea he suffered from obstructive apnea. He was mentally retarded with an IQ of 4 and mental age of 2 months. He could respond to his name, and was able to recognize familiar people. He was on G Tube feeding since he was two years old. He had a trach tube in place for breathing, and a sleep apnea monitor was connected to check his breathing and heart rate, while sleeping or
For both Atrial and Ventricular septal defect the size of the opening or hole affects how severe the child’s
his neurologic intensive care unit (NICU) stay, Y.W. was intubated and placed on mechanical ventilation, had a feeding tube inserted and was placed on tube feedings, had a Foley catheter to down drain (DD), and had multiple IVs inserted. He developed pneumonia 1 month after admission.
It also disproved previous theories on the cause of crush syndrome. Alfred was able to gain wide recognition in the medical community after Vivien and Alfred provided undeniable proof. By the mid 1930s, they began experimental work in vascular and cardiac surgery. This defied medical taboos against operating on the heart. A decade later, this work would see them saving a life at Johns Hopkins. While doing this work, Alfred and Vivien would give dogs the blue baby syndrome. They did this so that they could figure out ways to cure the blue baby syndrome. They did surgery on dog’s hearts in hopes it would reverse the effects and save them from dying. By 1940, Blalock was offered the position of Chief of Surgery. He requested that Thomas would accompany him. In infants that have blue baby syndrome, blood is shunted past the lungs and it deprives them of oxygen. This is also why they turn blue. To cure this defect, it was suggested that it might be possible to reconnect the pipes in some kind of way. This would be done to increase the level of blood flow to the lungs. On November 29th, 1944, an eighteen-month-old named Eileen Saxon was the first infant the procedure would be tried
Heredity plays a role in atrial septal defect because of gene abnormalities and environmental exposure that heighten the chance of a child inheriting it. Although most ASD occur by chance with no clear cause, scientists are still searching for a reason to why it occurs. Some symptoms of atrial septal defect after birth include recurrent respiratory or lung infections, trouble in breathing, feeling drained when feeding (infants), being out of breath when doing physically intensive activities, missed heartbeats, heart murmurs, swelling of limbs such as feet, legs, or stomach areas, or getting a stroke. Detection can be done during of after the baby is born. During pregnancy, it may be seen during an ultrasound but it usually depends on the size of the hole and its location. In many cases, ASD is not detected until adulthood, in which detection can be done through x-rays or physical examination which is done with a stethoscope to check for heart murmurs. Treatment may not be necessary in most cases of ASD as the hole in the septum closes during childhood but more severe cases will require treatment. Medications can be used to reduce the signs of symptoms and infections as well as aiding the heart to
The bad thing about the situation was that medically there was nothing more that could be done for this patient. All the family could do was to sit by his bedside and wait for their loved one take his last breath, and to be at peace.
Congenital left ventricular outpouching (LVO) is an uncommon perinatal diagnosis. Various terms used in the medical literature to describe the LVO are a source of perplexity. The novel classification developed in a recent review by Rad et al attempting to provide a clear differentiation of the mixed definitions based on anatomical and cardiac imaging data. Our report presents a case series of prenatal diagnosis of LVO. The application of Rad et al original classification and its impact on the patients’ outcome are discussed.
Congenital left ventricular outpouching (LVO) is a rare disorder in which a confined protrusion arises from the left ventricular (LV) free wall. The terms LV aneurysm, LV diverticulum, double-chambered LV and LV accessory chamber have been used interchangeably in the literature [1–9], however anatomical differences do exist between these terms [10]. LV aneurysm is an expansible thin-walled, usually fibrotic myocardium and pericardium, pouch contracting in asynchrony with the LV and has a wide communication with the LV cavity. Conversely, an LV diverticulum has three cardiac wall layers (endocardium, myocardium and pericardium), contracts in synchrony with the LV and has a narrow connection to LV. LV accessory chamber presents an entity that combines some criteria of both aneurysm and diverticulum. Its wall is similar to a diverticulum but it has a wide communication with the LV as an aneurysm. Lastly, double-chambered left ventricle displays a combination of the above-mentioned characteristics.
Cyanotic congenital heart defects include; Transposition of the great arteries, Truncus arteriosus, Total anomalous pulmonary venous connection. (5)
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.