Ventricular septal defect (VSD) and tetralogy of Fallout are heart defects ailment. The defects result from a gap in the ventricular septum (Corno, 2009). The gap lets oxygenated blood to combine with the non-oxygenated blood in the heart chambers (Abdulla, 2011). The two defects affect the functioning of the heart and are prevalent among infants.
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As ventricular contraction takes place, some blood in the left ventricle seeps out and enters into the right ventricle. Thereafter, the blood circulates through the lungs. From the lungs, the blood is passed through the left ventricle. Because of this, two net effects are created. The twisted outward flow of blood leads to increased volume in the left ventricle. Given that the left ventricle exhibits a higher systolic pressure compared to the right ventricle, then seeped out blood increases pressure in the right ventricles.
As a result, pulmonary hypertension occurs. In severe conditions, the pulmonary arterial pressure may increase to be in equilibrium with the systemic pressure. During such conditions, the left to right shunt is inverted. Owing to this, the blood seeps out from right to the left ventricle leading to a situation known as cyanosis. The above effect is more prominent in persons with larger defects.
Unlike the ventricular septal defect, tetralogy of Fallot is distinguished by four heart malfunctions. The malfunctions are the overriding aorta, ventricular septal defect, and right ventricular hypertrophy (Karl, 2008). Anatomic differences exist between the hearts of persons with the disease. As such, the extent of right ventricular outflow tract impediment differs between one individual to another.
The dissimilarities determine the disease’s signs. As such, the above differences are due to the imbalanced growth of the aorticopulmonary septum. In such a case, the aorta is too outsized. Due to this, the pressure levels required to be maintained between the vessel and that of the pulmonary artery is not maintained. The situation thwarts the ventricular wall closure.
Usually, VSD has no symptoms at birth. The symptoms are often manifested after some few weeks from the date of birth. During the early stages, cyanosis symptoms are not manifested. Nevertheless, if the defect is not corrected pulmonary resistance increases with time. Due to this, inversion of the shunt and related cyanosis occurs. In general, VDS’ symptoms include bluish hue on the patient’s skin, lips or fingernails cyanosis, loss of appetite, quick breathing, breathlessness, swelling of legs, swelling of the abdomen, and rapid heart rate.
Just like a ventricular septal defect, tetralogy of Fallot occurs when the blood with low oxygen levels is exposed to blood with high oxygen levels in the heart left ventricle chambers. The above situation happens due to a VSD. Tetralogy of Fallot’s major symptom is decreased blood oxygen saturation. The decreased blood oxygen is registered in the presence or absence of cyanosis.
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The above condition is normally developed from birth or within the firsts one year. When the baby shows no signs of cyanotic, the condition is known as pink tet. Like the VSD, tetralogy of Fallot’s signs may include heart murmurs. The murmurs may vary from almost being undetectable to be detectable. Other manifestations include loss of appetite, failure to gain weight, stunted growth, retarded physical development, dyspnea on exertion, clubbing of the patient’s feet, and polycythemia.
Infants with defects usually develop tet spells. The exact mechanism of these episodes is still unknown. However, it is thought that the condition results from a temporary increase in opposition to blood circulation to the lungs with an increased preferential circulation of de-saturated blood to the other body organs. Tet spells are manifested by an unexpected rise in cyanosis.
The condition may lead to hypoxic brain injury and death. Usually, grown-up children sit on their heels during a tet spell. Because of this, their systemic vascular resistance raises, enabling transitory reversal of the shunt.
Nursing medical management
In most cases, small VDS heal naturally during the infant’s first year. For infants, VDS is usually managed with cardiac glycosides medicine. However, larger VDS is treated through surgical or conservative interventions. A number of cases may require surgical treatment when they exhibit some indications.
The indications are lack of congestive cardiac to act in response to conservative medications, ventricular septal defect with pulmonic stenosis, pulmonary high blood pressure, and aortic regurgitation. Surgical procedures are conducted with the help of heart-lung machines. The machines allow doctors to carry out a median sternotomy.
When tetralogy of Fallot is detected in a child, the urgent intervention centers on establishing if the patient’s oxygen levels are in a harmless range. When oxygen levels are detected to be significantly lower during delivery, a prostaglandin infusion is undertaken. Through this, the ductus arteriosus is kept unlocked to offer extrapulmonary blood circulation and enhance the infant’s oxygen level.
Thereafter, the child should receive surgical treatment during his or her neonatal age. Infants who exhibit normal oxygen levels are discharged within their first week. Comprehensive repair is usually undertaken when the child is six months old, given that his or her blood oxygen levels remain sufficient. Progressive or abrupt reduction in the infant’s blood oxygen levels will require an advanced counteractive repair.
Surgical repair of the defect is always recommended. Usually, the infants will necessitate a surgical palliative intervention preceding to the last correction. Curative repair of the defects requires shutting off the VDS with an artificial Dacron patch. Through this, the blood can circulate as required in the heart chambers.
Ventricular septal defects are identified through cardiac auscultation. Naturally, the ventricular septal defect causes a pansystolic murmur. Auscultation is normally deemed adequate for identifying a number of VSDs (Wang, 2011). The murmur is caused by the unusual seepage of some blood from the left ventricle to the right ventricle. In the absence of adequate pressure difference between the two ventricles, the murmur might not be heard.
The above situation is normally experienced in infants with VSD after birth. With time, the difference between the two ventricles increases, leading to the development of the murmur. As such, cardiac auscultation must be verified. To achieve this, non-invasive cardiac ultrasound is required (Chessa, 2012). Similarly, to determine ventricular pressures with precision, cardiac catheterization is undertaken.
On the other hand, if left unattended, Tetralogy Of Fallot speedily leads to right ventricular hypertrophy. Hypertrophy results from increased blood resistance in the ventricles. The above may advance to heart failure. The heart failure starts in the right ventricle before proceeding to the left ventricle. Individuals who have gone through a comprehensive surgical repair have better hemodynamic.
Surgical achievement and long-term result largely rely on the specific anatomy of the patient and the doctor’s proficiency and experiences. More than 90% of patients with comprehensive repair as toddlers grow a gradually permeable pulmonary valve later in their middle ages (Moss & Allen, 2008). Therefore, the patients need regular follow up.
Abdulla, R. (2011). Heart diseases in children a pediatrician’s guide. New York: Springer.
Chessa, M. (2012). The right ventricle in adults with tetralogy of fallot. Milan: Springer.
Corno, A. F. (2009). Congenital heart defects decision making for cardiac surgery.. Darmstadt: Steinkopff.
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Karl, T. (2008). Tetralogy Of Fallot: Current Surgical Perspective. Annals of Pediatric Cardiology, 1(2), 93-99.
Moss, A. J., & Allen, H. D. (2008). Moss and Adams’ heart disease in infants, children, and adolescents: including the fetus and young adult. (7th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Wang, J. (2011). Transcatheter Closure of Ventricular Septal Defect and Atrial Septal Defect. Pediatrics & Neonatology, 52(5), 241-242.