Wait a second!
More handpicked essays just for you.
More handpicked essays just for you.
Personal opinion about hypoplastic left heart syndrome
Flash card on congenital heart diseases
Flash card on congenital heart diseases
Don’t take our word for it - see why 10 million students trust us with their essay needs.
1. Hypoplastic left heart syndrome (also called HLHS) is a congenital heart defect occurring during the first 8 weeks of pregnancy which leaves the left side of the heart underdeveloped and small. Normally, the right side flows blood to the lungs where oxygen is enriched before it travels to the heart’s left side while the left side of the heart pumps blood into the aorta which flows oxygen-rich blood to the body. In HLHS, the left side of the heart is not able to pump oxygen-rich blood to the body efficiently because the left ventricle is underdeveloped or small. In this case, the right side of the heart pumps the blood both into the lungs and the rest of the body through the ductus arteriosus and the oxygen-rich blood travels back to the …show more content…
Pulmonary atresia is congenital heart defect wherein the baby’s pulmonary valve does not form properly. Normally, the pulmonary valve regulates the blood flow from the heart to the lungs. In pulmonary atresia, a solid sheet of tissue forms at the valve opening which keeps the valve closed. Due to this, the blood from the right side of the heart cannot travel in its normal pathway to pick up oxygen from the lungs. Symptoms of pulmonary atresia may include cyanosis, rapid breathing, fatigue, poor nutrition, and shortness of breath. Possible treatments of pulmonary atresia include administration of prostaglandin E1, open heart surgery, heart reconstruction, heart transplant, and heart …show more content…
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that mostly affects premature infants. Premature infants have very few tiny alveoli that are not fully developed for the lungs to function normally. As a result, premature infants need respiratory support to provide oxygen or they need to be under mechanical ventilation in order to support their breathing. However, BPD is a result of the damage to the lungs caused by mechanical ventilation or by the long-term use of supplemental oxygen. This causes dysplasia and scarring of the air sacs and the damage will continue to affect alveoli that develop after birth. It will also affect the blood vessels which make it difficult for blood to go through the lungs, resulting in pulmonary hypertension and even heart failure. Most babies who have BPD are born with respiratory distress syndrome, a breathing disorder wherein fluid builds up in the alveoli which decreases the amount of oxygen reaching the bloodstream resulting in oxygen deprivation. The lungs are not completely formed or are unable to produce adequate surfactant, the liquid that covers the lungs in order to keep them open and aid in breathing once the infant is born. Without adequate surfactant, the lungs can collapse which causes difficulty in breathing. Because of this, the infant is not able to breathe and circulate sufficient levels of oxygen in order to support the other organs of the body. Most common symptoms of BPD are rapid and labored breathing,
Ebstein’s Anomaly is a rare congenital condition, present at birth, in which the tricuspid valve is malformed and the valve itself is not in the correct anatomic place (Mayo Clinic Staff). This anomaly affects the right side of the heart – the tricuspid valve is located too deep into the ventricle, causing a smaller and weaker right ventricle. The space above the decreased right ventricle is made up of atrial tissue and this can be referred to as right ventricle dysplasia or an atrialized right ventricle (Reynolds). Typically the tricuspid valve has three freely moving leaflets, but in Ebstein’s anomaly one or two of those leaflets get fused to the heart walls causing regurgitation. Since the heart does not work as efficiently in those who have this anomaly, the heart usually compensates and becomes enlarged. It...
“Hypoplastic left heart syndrome accounts for 9% of all critically ill newborns with congenital cardiac disease, causing the largest number of cardiac deaths in the first year of life.(2) ” HLHS is a severe heart defect that is present at birth. HLHS combines different defects that result in an underdeveloped left side of the heart. This syndrome is one of the most challenging and difficult to manage of all of the congenital heart defects. Multiple portions on the left side of the heart are affected including the left ventricle, the mitral and aortic valve, and the ascending aorta. These structures are greatly reduced in size, or completely nonexistent causing the functionality of the left heart to be reduced, or non-functional all together.
The thickening of the muscle cells do not necessarily have to change the size of the ventricles, but can narrow the blood vessels inside the heart. Hypertrophic cardiomyopathy can be grouped into two categories: obstructive HCM and non-obstructive HCM. With obstructive HCM, the septum (the wall that divides the left and right sides of the heart) becomes thickened and blocks the blood flow out of the left ventricle. Overall, HCM usually starts in the left ventricle. HCM can also cause blood to leak backward through the mitral valve causing even more problems. The walls of the ventricles can also become stiff since it cannot hold a normal amount of blood. This stiffening causes the ventricle to not relax and entirely fill with
Chronic obstructive pulmonary disease or COPD is a group of progressive lung diseases that block airflow and make it hard to breathe. Emphysema and chronic bronchitis are the most common types of COPD (Ignatavicius & Workman, 2016, p 557). Primary symptoms include coughing, mucus, chest pain, shortness of breath, and wheezing (Ignatavicius & Workman, 2016, p.557). COPD develops slowly and worsens over time if not treated during early stages. The disease has no cure, but medication and disease management can slow its progress and make one feel better (NIH, 2013)
First and foremost, Eisenmenger syndrome was initially described in 1897 when German physician, Victor Eisenmenger, reported on a patient with symptoms of dyspnea and cyanosis from infancy that subsequently developed heart failure (Connolly, 2014). The postmortem description was revealed and a ventricular septal defect was discovered (El-Chami et al., 2014a). With that being said, this had been the first time that the link between a large congenital cardiac shunt defect and the development of pulmonary hypertension had ever been noted (El-Chami et al., 2014b). The normal heart has four chambers. The two upper chambers are separated from each other by the atrial septum (NORD, 2014a). The two lower chambers are known as ventricles and are separated from each other by the ventricular septum (NORD, 2014b).
According to Batshaw, Roizen, and Lotrecchiano (2013), patent ductus arteriosus (PDA) is “the persistence of a fetal passage permitting blood to bypass the lungs” (p. 745). This is an inherited heart condition in which the ductus, a small pathway between the pulmonary and the aortic, valves remain open. This cardiovascular problem usually occurs in low birth weight infants. The blood vessels usually naturally closes after birth (Batshaw et al., 2013, p. 96). It becomes atypical if it remains open after the neonatal period. The structure usually closes in typical developing newborns around the initial 24 hours, and anatomical closure is supposed to follow several weeks later (Stanford Children’s Health, 2015). At the point when the ductus arteriosus stays open, the blood from the oxygen-rich aorta blends with the oxygen-poor pulmonary artery causing the higher chance of blood pressure in the lung pathways (U. S. Department of Health and Human Services, 2011). Certain children who have patent ductus arteriosus may be given medication, relying upon the circumstance to standardize the blood and oxygen levels until surgery is performed. Doctor can treat this condition by providing pharmaceutical medicine, catheter-based procedures, and surgery (U. S. Department of Health and Human Services, 2011).
Healthy lung tissue is predominately soft, elastic connective tissue, designed to slide easily over the thorax with each breath. The lungs are covered with visceral pleura which glide fluidly over the parietal pleura of the thoracic cavity thanks to the serous secretion of pleural fluid (Marieb, 2006, p. 430). During inhalation, the lungs expand with air, similar to filling a balloon. The pliable latex of the balloon allows it to expand, just as the pliability of lungs and their components allows for expansion. During exhalation, the volume of air decrease causing a deflation, similar to letting air out of the balloon. However, unlike a balloon, the paired lungs are not filled with empty spaces; the bronchi enter the lungs and subdivide progressively smaller into bronchioles, a network of conducting passageways leading to the alveoli (Marieb, 2006, p. 433). Alveoli are small air sacs in the respiratory zone. The respiratory zone also consists of bronchioles and alveolar ducts, and is responsible for the exchange of oxygen and carbon dioxide (Marieb, 2006, p. 433).
Cardiofaciocutaneous syndrome is a very rare and serious genetic disorder that generally affects the heart, facial features, and skin of an individual. It is caused by a desultory gene mutation, which takes place in one of four genes. Those genes are known as BRAF, MEK1, MEK2, and KRAS. From research, it is also suspected there is a possibility that other genes are associated with the rare condition. This disorder holds multiple alternative names, a long history, obvious symptoms, extensive amounts of interesting data, and is lucky enough to be supported by numerous organizations that will stop at nothing to help.
Tetralogy of Fallot is a congenital heart disease which involves four different heart defects in one. The four different heart defects are a large ventricular septal defect (VSD), Pulmonary Stenosis, Right ventricular hypertrophy, and an overriding aorta. These congenital defects change the normal flow of blood thro...
Chronic obstructive pulmonary disease (COPD) is preventable disease that has a detrimental effects on both the airway and lung parenchyma (Nazir & Erbland, 2009). COPD categorises emphysema and chronic bronchitis, both of which are characterised by a reduced maximum expiratory flow and slow but forced emptying of the lungs (Jeffery 1998). The disease has the one of the highest number of fatalities in the developed world due to the ever increasing amount of tobacco smokers and is associated with significant morbidity and mortality (Marx, Hockberger & Walls, 2014). Signs and symptoms that indicate the presence of the disease include a productive cough, wheezing, dyspnoea and predisposing risk factors (Edelman et al., 1992). The diagnosis of COPD is predominantly based on the results of a lung function assessment (Larsson, 2007). Chronic bronchitis is differentiated from emphysema by it's presentation of a productive cough present for a minimum of three months in two consecutive years that cannot be attributed to other pulmonary or cardiac causes (Marx, Hockberger & Walls, 2014) (Viegi et al., 2007). Whereas emphysema is defined pathologically as as the irreversible destruction without obvious fibrosis of the lung alveoli (Marx, Hockberger & Walls, 2014) (Veigi et al., 2007).It is common for emphysema and chronic bronchitis to be diagnosed concurrently owing to the similarities between the diseases (Marx, Hockberger & Walls, 2014).
Hypertrophic cardiomyopathy is an inherited disease that affects the cardiac muscle of the heart, causing the walls of the heart to thicken and become stiff. [1] On a cellular level, the sarcomere increase in size. As a result, the cardiac muscles become abnormally thick, making it difficult for the cells to contract and the heart to pump. A genetic mutation causes the myocytes to form chaotic intersecting bundles. A pathognomonic abnormality called myocardial fiber disarray. [2,12] How the hypertrophy is distributed throughout the heart is varied. Though, in most cases, the left ventricle is always affected. [3] The heart muscle can thicken in four different patterns. The most common being asymmetrical septal hypertrophy without obstruction. Here the intraventricular septum becomes thick, but the mitral valve is not affected. Asymmetrical septal hypertrophy with obstruction causes the mitral valve to touch the septal wall during contraction. (Left ventricle outflow tract obstruction.) The obstruction of the mitral valve allows for blood to slowly flow from the left ventricle back into the left atrium (Mitral regurgitation). Symmetrical hypertrophy is the thickening of the entire left ven...
The clinical manifestation one may see in patients with chronic bronchitis are chronic cough, weight loss, excessive sputum, and dyspnea. Chronic cough is from the body trying to expel the excessive mucus build up to return breathing back to normal. Dyspnea is from the thickening of the bronchial walls causing constriction, thereby altering the breathing pattern. This causes the body to use other surrounding muscles to help with breathing which can be exhausting. These patients ca...
Just as breast cancer is killing our African American women, heart disease is also one of the major diseases killing our women. Heart disease is one of the nation’s leading causes of death in both woman and men. About 600,000 people die of heart disease in the United States (Americas heart disease burden, 2013). Some facts about heart disease are every year about 935,000 Americans have a heart attack. Of these, 610,000 are a first heart attack victim. 325,000 happen in people who have already had a heart attack. Also coronary heart disease alone costs the United States $108.9 billion each year. This total includes the cost of health care services, medications, and loss of productivity. Deaths of heart disease in the United States back in 2008 killed about 24.5% of African Americans.
Parker, Steve. "Chronic Pulmonary Diseases." The Human Body Book. New ed. New York: DK Pub., 2007.
This obstruction inhibits the exchange of oxygen and carbon dioxide. COPD is not one singular disease, rather it includes all diseases which makes it difficult to breath. These diseases include emphysema, chronic asthma and bronchitis to name a few. Emphysema is a COPD disease in which the lungs lose elasticity, or their ability to stretch and expand. This reduction in elasticity eventually caused the break-down of lung tissue. Without the lungs ability to expand the air breathed in cannot be fully expelled, which causes less oxygen to be able to enter. Eventually carbon dioxide fills the lungs, and causes the patient to feel stressed and like they are suffocating. The alveoli of the lungs begin to fuse together and form large air sacs. These sacs eventually rupture allowing air to fill the spaces between the lungs and the chest. This is called pneumothorax, and this condition will cause the lungs to collapse due to the increased pressure. Emphysema can be inherited, or caused by smoking. No other cause is known for this disease. Bronchitis is another COPD disease which is the swelling of the bronchi. The mucous glands produce a large amount of mucus. This mucus and inflammation of the mucosa causes blockage in the airway, and inhibits the body from receiving enough oxygen. The low amount of oxygen in the body is called