“VSD (Ventricular Septal Defect)” refers to a defect in the heart. VSD is characterized by one or more holes in the septal wall. This wall separates the two ventricles (right and left). On the other hand, “ToF (Tetralogy of Fallot)” is a condition of the heart that occurs at birth. ToF combines four defects, namely “VSD, RVH (right ventricular hypertrophy), and (APoA) abnormal position of the aorta and (PS) pulmonary valve stenosis.” This paper will compare and contrast VSD and ToF (Webb, Smallhorn, Therrien, & Redington, 2011).
VSD allows for communication between the pulmonary and systematic circulations. This makes flow to travel from a part of high to low pressure. These changes are derived from changes in the pulmonary vasculature and left to right shunt. The latter effect has the following consequences; increased LV volume load, excessive pulmonary blood flow, and reduced systematic cardiac output.
VSD can lead to spontaneous closure or congestive heart failure (CHF) or death at infancy level. The former can happen by the age of two. The most common type of closure is muscular defect followed by the perimembranous defect. VSD patients are usually at risk of endocarditis.
On the other hand, ToF occurs as one of the conotruncal malformations. ToF is usually associated with CATCH 22 since it demonstrates deletions of part of chromosome band known as DiGeorge critical region. “Hemodynamics” of ToF relies mainly on the extent of RVOTO “outflow tract obstruction of the right ventricle.” It is necessary to note that VSD is usually non-restrictive; this can allow for equalization of pressures in the right ventricle and left ventricle.
Therefore, in the case of severe obstruction, pulmonary blood flow may be restricted too. It can be noted form the pathophysiology that although VSD differs from ToF, they are closely linked in that VSD form part of ToF. Additionally, it should be noted that the two defects concern both the right and left ventricular pressures.
Additionally, they are both congenital defects of the heart. However, ToF is usually more complex to given that it involves VSD and PS, among other defects, as stated above. Children that suffer from VSD or ToF are both at risk of attracting diseases that affect layers of the heart. Such conditions include endocarditis, among others (Mølgaard-Nielsen, Pasternak, & Hviid, 2013).
VSD patients rarely show clinical manifestations. Nonetheless, this is possible when the hole is large. Some of the clinical manifestations of VSD include “short breath, paleness, increased heart rate, difficulty in breathing, reduced ability to add weight and increased the frequency of breath.” Others include frequent respiratory infections and sweating whenever eating. On the other hand, children with ToF are prone to chromosome disorders. These may include DiGeorge and Down syndromes.
Clinical manifestations in children with ToF include “cyanosis (this makes the skin of a child blue), bulging of bone or skin in the region of fingernails, inability to add weight, squatting whenever cyanosis occurs, poor development and passing out.” It should also be noted that patients with ToF might have higher risks of acquiring other infections such as endocarditis. Additionally, such patients can experience dizziness and delayed growth, which results from low oxygen levels in the blood.
It can be noted that patients with VSD and ToF have some similarities in clinical manifestations. These include failure of the patients to gain weight and delayed development. However, a number of differences can also be noted in clinical manifestations. For instance, while children with ToF may have blue skins, those with VSD look pale (Szkutnik, Kusa, & Bialkowski, 2008).
Both defects require medical attention. However, this depends on the kind of clinical manifestations observed. For instance, when a child’s body turns blue, he/she should be placed on his/her back (knee to chest position) immediately. This is important in increasing aortic resistance. If it happens at home, the guardian should seek medical attention immediately.
Various medications can be offered for children with ToF. However, the most basic medication offered is a surgery that corrects the heart problem. Other management measures may include giving the child oxygen through masks or other medications such as morphine, among others to reduce the frequency or severity of tet spells.
Similarly, management of VSD can be done when a large hole occurs, which cause clinical manifestations. However, it should be noted that the kind of medication prescribed rely heavily on the extent of clinical manifestations. In most cases, therapy is done to minimize clinical manifestations of CHF. These may include weight gain, fast breathing, fluid in lungs and weight loss, among others. Medical management of VSD should also ensure that the infection does not spread into endocarditis.
Other medications, which can be utilized, include Vasodilators, among others. In some cases, large VSDs require surgical closure, especially if medications are not working. It can be noted that both congenital defects require surgery, especially ToF.
Only large VSD may require surgical closure. However, the management of ToF is more complex than the management of VSD since it can lead to CHF. Nonetheless, both defects require close monitoring (follow up) to ensure that clinical manifestations are minimized (Predescu, Chaturvedi, Friedberg, Benson, Ozawa, & Lee, 2008).
Children with small holes have good prognoses in the long term. However, those with large holes have varying outcomes, which depend on the severity of their conditions. However, previous medical therapy has shown improvements in infants between half and two-year-olds.
This happens because of the gradual decrease in left to right shunt. It has also been observed that most babies with VSD get better or stay in steady condition after infancy. However, respiratory infections and other heart defects such as endocarditis can lead to clinical manifestations. Surgical mortality is also low (below 2%). However, lung or heart transplantation is also possible for some VSD patients.
Conversely, surgery is essential for infants with ToF. In fact, the lack of surgery has shown poor prognosis. Nonetheless, it should be noted that prognosis relies mainly on the extent of RVOTO. Children with uncomplicated types of ToF usually go through cardiac surgery, which has shown good prognosis as well as promising futures for patients. Fatalities that happen later in life have been observed to be about 5%. This happens due to “ventricular arrhythmias.”
However, to minimize such occurrence, patients should be taken through “cardiac monitoring” until adulthood. It should also be noted that if ToF is ignored, then another risks such as stroke and endocarditis could be developed. Moreover, if surgery is ignored, death rates can swell from 30% to 60%. This is most prevalent between the ages of 2 and six years, respectively. It can be noted that VSD shows good prognosis than ToF if surgery is ignored (Shepard, Tejman-Yarden, Khanna, Davis, & Batra, 2011).
Both VSD and ToF are congenital defects, which begin at birth. While VSD is characterized by a hole in the septal wall of the heart, disordered chromosomes characterize ToF. It is important to note that VSD is one of the four defects of the heart that make up ToF. Moreover, while surgery is necessary for good prognosis of ToF patients, it is only a requirement for large VSDs (Marinho, Alho, Guerra, Rego, Areias, & Bicho, 2009).
Marinho, C., Alho, I., Guerra, A., Rego, C., Areias, J., & Bicho, M. (2009). The methylenetetrahydrofolate reductase gene variant (C677T) as a susceptibility gene for tetralogy of Fallot. Rev Port Cardiol. 28(7-8), pp. 809-812.
Mølgaard-Nielsen, D., Pasternak, B., & Hviid, A. (2013). Use of oral fluconazole during pregnancy and the risk of birth defects. N Engl J Med., 369(9), pp. 830-839.
Predescu, D., Chaturvedi, R., Friedberg, K., Benson, L., Ozawa, A., & Lee, J. (2008). Complete heart block associated with device closure of perimembranous ventricular septal defects. J Thorac Cardiovasc Surg.136(5), pp. 1223-1228.
Shepard, S., Tejman-Yarden, S., Khanna, S., Davis, C., & Batra, S. (2011). Dexmedetomidine-related atrial standstill and loss of capture in a pediatric patient after congenital heart surgery. Crit Care Med.39(1), pp. 187-189.
Szkutnik, M., Kusa, J., & Bialkowski, J. (2008). Percutaneous closure of perimembranous ventricular septal defects with Amplatzer occluders–a single centre experience. Kardiol Pol., 66(9), pp. 941-949.
Webb, G., Smallhorn, J., Therrien, J., & Redington, A. (2011). Congenital heart disease. In M. D. Bonow RO, Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. (chap. 65). Philadelphia, PA: Saunders Elsevier.