Aneurysm Report

The left side of the heart appeared slightly bigger than the right side. The atria looked like flaps and were very flimsy compared to the ventricles. The ventricles appeared light pink in colour and were very big, taking up a lot of space in the heart. The arteries were identified, but the veins were not. A finger could be placed down the aorta.

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.

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

R E V I E W S H E E T 30 Anatomy of the Heart

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.

Cardiovascular Assessment: No visible pulsations, no heaves or lifts. Apical pulse present in the fifth intercostal space at the left midclavicular line. Auscultation of apical rate 62 beats per minute, normal rhythm regular S1 - S2 heart sounds present. Pulsations present when supine and disappear at a 45 degree angle position. Extremities are brown color without redness, cyanosis, lesions or varicosities bilaterally. Temperature warm bilaterally, Allen test was negative. Homan’s sign negative. Carotids: +2 and present bilaterally. Right Radial +2, left radial +1 , Right Brachial: +2

For this myocardial infarction, the right coronary artery was blocked. The parts of the heart that were affected by this blockage was the right atrium, the right ventricle, the interventricular septum, the Sinoatrial node and the AV node, and some parts of the left atrium and ventricle. These parts were affected because the right coronary artery supplies blood to these parts of the heart; since there was a blockage the blood was not able to continue through the right coronary arteries into its branches, which are the sinoatrial nodal artery, the right marginal branch, the posterior interventricular branch, and the atrioventricular nodal artery (Gest).

Since the age of seven I have been fighting what many think is the impossible. When I was seven I was diagnosed with a ruptured aneurysm and an arteriovenous malformation also know as a AVM. My case wasn't rare in the case of a ruptured aneurysm but was rare in the case that such a young child had a ruptured aneurysm. I was a lost cause in what many doctors told my mom, in a last ditch effort to save my life I was life-flighted to Iowa University Hospitals where a doctor took a chance on my life when no one else would and he was able to save my life. I had beat the impossible that I was still alive and wasn't dead, not in a wheelchair, could still talk, I was able to feed my myself. It was a long journey through, constant doctor visits

Even when these patients are brought in exhibiting these symptoms, due to the rarity of Uhl’s anomaly, all other possibilities are researched first. Often after echocardiography, chest x-rays, and EKG’s are done, and treatment is administered, there is usually minimal or no

Echocardiography: The position of valves is fit. The size and movements of the valve are reasonable. There is no problem in her valves. The velocity of blood flow is appropriate.

An AAA (abdominal aortic aneurysm) is defined as enlargement of at least 3 cm of the abdominal aorta. The majority of abdominal aortic aneurysms begins below the renal arteries and ends above the iliac arteries. The exact cause of (AAAs) is unknown. However, it is thought to be due to a degenerative process of the abdominal aorta caused by atherosclerosis. Artherosclerosis represents a response to vessel wall injury caused by inflammation, genetically regulated defects in collagen and fibrillin, increased protease activity within the arterial wall, and mechanical factors (Stoelting p. 143).

Pericardial effusion appears as anechoic stripe that is surrounding heart (Fig.26). Smaller effusions appear as a thin stripe in the pericardial space, frequently not spreading fully around the heart and often layering out posteriorly with gravity

Right ventricular infarction may occur with occlusion of the right coronary artery. With infarct affect the posterior wall of the left ventricle and the posterior interventricular septum, they extend to the right ventricular wall in 15 to 30% of cases. The central venous pressure may be elevated markedly if acute right ventricular failure develops. Low right ventricular output causing shock often responds well to vigorous fluid therapy but poorly to vasodilators. Infusions raise both right and left ventricular filling pressures. The diagnosis of right ventricular infarction is difficult but may be established by right sided ECG leads and echocardiographic studies (Bullock, 1996).

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)