A ventricular septal defect (VSD) is a hole or a defect in the septum that divides the two lower chambers of the heart, leading to a connection between left and right ventricle (Dittrich, Ewert, Le, & Horer, 2010), while tetralogy of fallot (TOF) is the most common cyanotic congenital heart defect in all age groups which causes the mixing of oxygen-poor blood with oxygen-rich blood being pumped from the heart into the circulatory system of blood vessels (British Heart Foundation, 2008). This paper compares and contrasts the two heart conditions in terms of their ‘pathophysiology, clinical manifestations, nursing/medical management, as well as prognosis.’
It is important to note that VCD not only allows shunting of blood from the left ventricle (high pressure) to the right ventricle, but most of the shunts normally occur at the level of the outflow tracts and the overloaded pulmonary circulation enhances return of blood to the left atrium and ventricle. Available scholarship also demonstrates that pulmonary hypertension may initialize in huge VCDs, leading to a pressure overload of the right ventricle and subsequent compensatory hypertrophy (Dittrich et al 2010). However, a trend has been observed whereby fairly huge VCDs trigger left atrial and ventricular volume overload as well as left-sided congestive heart failure, leading to serious heart abnormalities in the absence of proactive strategies to correct the situation. In contrast, the pathophysiology of TOF is dictated by three anatomical factors namely (1) degree of right ventricular outflow tract obstruction, (2) pulmonary artery anatomy, and (3) non-restrictive mal-alignment VSD (Gatzoulis & Murphy, 2001). It should be noted that VSD represents one of the four abnormalities described by TOF, with the other abnormalities including right ventricular hypertrophy, abnormal position of the aorta, and pulmonary valve stenosis. This implies that VSD is always present in incidences of TOF, necessitating a condition where the hole in the heart wall (septum) allows oxygen-poor blood in the right ventricle to pass through and mix with oxygen-rich blood in the left ventricle (British Heart Foundation, 2008). From this exposition, it can be further deduced that both VSD and TOF are serious heart abnormalities that require a surgical procedure to correct.
The symptoms associated with VSDs are to a large extent dependent on the size of the defect and the magnitude of the left-to-right shunt, and include systolic heart murmur due to failure of pulmonary resistance, congestive heart failure arising from the extension of left-to-right shunt, and increase in the intensity of heart sound (Dittrich et al 2010). Although available literature demonstrates that heart murmur might substantially diminish if pulmonary resistance rises in large non-restrictive VSD, the disease might prove irreversible even after six months of age due to pulmonary vascular remodeling (Caputo et al., 2005). The disease may prove fatal owing to the fact that the right-to-left shunt is initiated after some years. In contrast, most clinical manifestations of TOF are directly related to the low level of oxygen in the patient’s blood arising from the mixing of oxygen-poor blood with oxygen-rich blood in the ventricles. Available scholarship demonstrates that most patients with TOF appear blue particularly on the lips, tongue, hands and mouth, not mentioning that some patients experience hypercyanotic attacks which make them appear floppy or faint (British Heart Foundation, 2008). As is the case with VSD, these attacks can be very serious and may even prove fatal if necessary corrective action (surgery) is not commenced.
In VSD, it is suggested that chest radiography, magnetic resonance imaging (MRI), and electrocardiography (ECG) may be used by nursing/medical personnel to avail important information related to the workup of a VSD variant; however, detailed echocardiography is now preferred as a standard model of VSD evaluation (Dittrich et al 2010). Young children with small VSDs are asymptomatic and demonstrate an outstanding long-term prognosis, thus no medical therapy or surgical therapy should be indicated. In children with modest or huge VSDs, nursing/medical professionals should indicate a trial of medical therapy with the view to effectively managing symptomatic congestive heart failure (Caputo et al., 2005). Nurses and medical professionals should understand that uncontrolled congestive heart failure and recurrent infection which characterize VSD are often indicative of surgical repair (Caputo et al., 2005), and that age, size of the patient, or prior use of anti-congestive medication should not be used to blacklist surgery as the best management/treatment option (Dittrich et al 2010). In a marked similarity, nursing professionals need to assess the patient using an echocardiogram to make the diagnosis of TOF, not to mention that surgery is the preferred mode of treatment/management of the condition. Nursing/medical professionals should however note that any person who has undergone a tetralogy repair operation will have an irregular or uncharacteristic pulmonary valve that does nor close effectively, not only causing the right ventricle to work harder than usual but also triggering an enlargement of the ventricle as the years go by (British Heart Foundation, 2008). Consequently, unlike in VSD where a single operation may be effective, patients suffering from TOF often require further surgery as the year’s progress to replace the valve.
In the prognosis of VSD, it is documented that (1) pulmonary arterial hypertension with the occurrence of right-to-left-shunt (pulmonary vascular obstructive disease) is responsible for initiating Eisenmenger’s syndrome, (2) spontaneous downsizing and closure of perimembranous and muscular VSD are frequent during the first years of life and even occur in adults with perimembranous VSD, (3) normal life-span for patients suffering from some variants of VSD can be achieved with timely therapy, (4) medications are often unable to effectively treat VSD in the absence of surgery, and (5) VSD may aggravate TOF and lead to undesirable outcomes if repair-oriented surgery is not conducted to patch the hole in the heart wall which is responsible for allowing oxygen-poor blood in the right ventricle to pass through and mix with oxygen-rich blood in the left ventricle, leading to cyanosis due to lack of adequate oxygen in the blood (Dittrich et al 2010). The prognosis of TOF demonstrates that the heart condition may not be life-threatening in newborn babies and young children, though medications cannot be used to correct the condition even when the patient is young. As is the case with VSD, TOF can only be corrected through surgery and other post-operative alterations. However, with the right kind of treatment/management, individuals suffering from TOF have a substantially high chance of achieving full recovery (Gatzoulis & Murphy, 2001).
Overall, this paper has successfully compared and contrasted two heart conditions (VSD and TOF) in terms of their ‘pathophysiology, clinical manifestations, nursing/medical management, as well as prognosis.’ It has been established that both diseases arise from dissimilar defects of the heart, though VSD is normally present in TOF. It has also been established that the two conditions can only be corrected through surgery and are normally diagnosed using echocardiography. Finally, it has been established that both diseases provide patients with an opportunity to make full recovery if proper corrective procedures are taken to address the conditions. However, TOF may require more than one surgery to successfully correct.
British Heart Foundation. (2008). Understanding your child’s heart: Tetralogy of fallot. Web.
Caputo, S., Capozzi, G., Russo, M.G., Esposito, T., Martina, L., Cardaropoli, D…Calabro, R. (2005). Familial recurrence of congenital heart disease in patients with ostium secundum atrial septal defect. European Heart Journal, 26(2), 2179-2184.
Dittrich, S., Ewert, P., Le, T.P., & Horer, J. (2010). Single ventricular septal defect (VSD). Web.
Gatzoulis, M., & Murphy, D. (2001). The adult with tetralogy of fallot: The ISACCD monograph series paperback. New York, NY: International Society of Adult Congenital Cardiac Disease.