Heart and Cardiovascular Function - Essay Example

of the of the Human anatomy 29 May Heart and Cardiovascular Function Nearly of children are born with congenital heart defects. These are caused due to genetic and environmental factors and their complex interactions. The abnormality is usually an aberrantly developed embryonic tissue or developmental arrest of a cardiac structure or tissue at an embryonic or fetal stage. Sometimes, these are a part of the profile of syndromes such as Down’s, Turner’s or other trisomies (Lilly 369-384).Congenital heart diseases (CHD) can be classified in to cyanotic and acyanotic heart disease.

In cyanotic heart disease there is mixing of the arterial oxygenated blood with desaturated venous blood. All cyanotic heart diseases are considered serious and should receive specialized care. Some of the complex cyanotic cardiac lesions involving multiple defects are tetrology of fallot, transposition of great arteries and Ebstein anomaly. Patients develop growth retardation, very limited activity and exercise tolerance, erythrocytosis and hyperviscosity syndrome (Lilly 380). Eisenmenger syndrome is the development of right to left shunt with pulmonary hypertension.

It carries a high risk of mortality (Lilly 384). Also, most of the individuals with congenital heart defects require infective endocarditis prophylaxis before any invasive procedure or surgery. Acyanotic diseases can be further classified as ‘with shunt’ or ‘without shunt’. Common acyanotic heart diseases with shunt are atrial septal defect (ASD), ventricular septal defect (VSD) and patent ductus arteriosus (PDA). Acyanotic heart diseases without shunt are congenital aortic stenosis (AS), coarctation of aorta and pulmonary stenosis with an intact ventricular septum (Lilly 370).

These defects can be diagnosed on history, clinical examination and imaging studies. Many of them are amenable to surgical treatment. Symptoms in adulthood depend upon the type and extent of repair attempted. Latest research in this area is being conducted around the early diagnosis and early treatment of these defects (Delgado-Olguín 343-347). Genetic linkage of many has been identified and fetal heart repair is being attempted.Works citedDelgado-Olguín, Paul, et al. “Epigenetic repression of cardiac progenitor gene expression by Ezh2 is required for postnatal cardiac homeostasis.

” Nature Genetics 44 (2012): 343-347.Lilly, Leonard S. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Philadelphia: Lippincott Williams & Wilkins, 2011.