Ventricular Septal Defect: Diagnosis and Treatment

Adunola Iyinolakan

Holly Jones-Taggart

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Ventricular Septal Defect

Ventricular septal defect is a structural heart defect and one of the most common congenital cardiac malformations caused by an opening in the intraventricular septum-the wall between the ventricles (lower chambers of the heart) that causes a left-to-right ventricular shunt of blood through the septum. VSDs can be congenital or acquired; they may be single or multiple and vary in size, location and clinical presentation; this variance helps in its diagnosis, treatment and prognosis. Anatomically, the ventricular septum is made up the membranous septum – which is made up of thin fibrous tissue at the superior part of the septum and the muscular septum-which is mainly muscles at inferior part of the septum, with three components: the inlet septum, the trabecular septum, and the outlet (or infundibular) septum. Defects in the membranous septum often extend into the muscular septum, these are called the perimembranous defects. The membranous defects make up the majority of VSDs- though they almost invariably also involve the muscular septum. VSD appears either as an isolated cardiac defect or with several complex malformations such as pulmonary hypertension, pulmonary stenosis or aortic regurgitation- which all play a role in the pathophysiologic consequence of the disease. This review will cover anatomy of VSD, with a focus on the diagnosis and treatment options available as seen from the authors’ point of view and in related reviews of Ventricular Septal Defect.

Heart Anatomy-The Ventricles

The heart has four chambers: a right and left upper atria which are separated by the atrial septum and a right and left lower ventricles which are separated by the ventricular septum. The septum prevents mixing of blood between the two sides of the heart. In normal heart function, oxygenated blood is ejected from the left ventricles through the aorta to the rest of the body. With VSD in early systole, ejected oxygenated blood from the left ventricle (LV) will be shunted through the VSD into the right ventricle where it mixes with deoxygenated blood. Hence oxygenated blood is pumped back to the pulmonary circuit instead of the body.   

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Diagnosis

Auscultation: Most VSDs are identified by auscultation depending on its size; location; and associated complications. Small or restrictive defects are associated with a palpable thrill in the third or fourth intercostal space. VSD produces a loud pathognomonic holosystolic or pansystolic murmur, heard best at Erb’s point. Small defects are often asymptomatic due to mild ventricular outflow or shunt lesion. Large defects however leads to an increase in mitral inflow which could generate a diastolic rumble at the apex.

Electrocardiography: Electrocardiogram (ECG) reflect the hemodynamic changes by coping the shunt size and the extent of pulmonary hypertension. Restrictive VSDs usually produce a normal tracing, a wide notched P wave due to left atrial overload is the characteristic of Medium-sized VSDs produce, and large VSDs shows hypertrophy of the right ventricle with right-axis deviation. With further progression of the defect, the ECG shows biventricular hypertrophy; P waves may be notched or peaked. This techniques is limited because small defects are difficult to image; and hence, only visualized by means of color Doppler examination.

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Echocardiography: Echocardiography evaluate the anatomy and physiology of the heart using sound waves to determine the size, pattern and volume of blood flow through the VSD. Two-dimensional (2D) and Doppler color-flow mapping are used to identify VSD type. Septal dropout in the area adjacent to the septal leaflet of the tricuspid valve and below the right border of the aortic annulus are seen in Perimembranous VSDs. Muscular defects may appear anywhere throughout the ventricular septum. The anatomic localization of all VSDs is facilitated by coupling 2D sonograms with a Doppler system and by overlaying a color-coded direction and velocity of blood flow on the real-time images.

Chest radiography: The chest radiograph reflects the magnitude of the shunt and the extent of pulmonary hypertension. Patients with a small VSD have a normal cardiac outline and pulmonary vascularity. Medium-sized VSDs, show minimal enlargement and a borderline increase in pulmonary vasculature; in large VSDs, the chest radiograph shows comprehensive hypertrophic cardiomyopathy with prominence of both ventricles, the left atrium, and the pulmonary artery. The pulmonary vascular markings are increased, and frank pulmonary edema, including pleural effusions, may be present. Cardiac catheterization: Angiography assesses pulmonary vascular resistance (PVD) of complicated VSDs. It is only performed when: (a) uncertain about shunt size after clinical evaluation; (b) laboratory data contradicts clinical findings; or (c) PVD is suspected. Oximetry show high level of oxygen in the right ventricle due to streaming (blood ejection almost directly into the pulmonary artery). Small VSDs are connected with normal right-sided heart pressures and pulmonary vascular resistance. Large, nonrestrictive VSDs are characterized by equal or near-equal pulmonary and systemic systolic pressures. Pulmonary blood flow may be two to four times above the systemic blood flow.

Magnetic Resonance Imaging: The current clinical role of MRI is to supplement the information acquired with echocardiography. The volumes, mass, and function of ventricles may be assessed by using cine MRI. Shunts volume, valvular function, and pressure gradients across the valves and conduits may be projected by the use of velocity-encoded cine MRI (velocity-flow mapping). In studies in which the results of MRI were corroborated with those of angiography and/or 2D echocardiography, an accurate anatomic diagnosis of anomalies was mostly achieved.

Treatment Options

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Medical Management: Small sized VSDs are often asymptomatic and need no medical treatment, but monitoring. However, treatment for large VSDs include –

1. Increased caloric density of feedings to ensure adequate weight gain/growth in babies.
2. Angiotensin-converting enzyme inhibitors to reduce afterload in systemic and pulmonary pressures (the former to a greater degree), thereby reducing the left-to-right shunt.
3. Digoxin can also be given for its inotropic effect- to increase the strength of the heart’s contractions and keep the heartbeat regular.
4. Diuretics such as furosemide is administered to relieve pulmonary congestion – long-term use of furosemide results in hypercalciuria, renal damage, and electrolyte disturbances.
5. Antibiotics-administered to patients whose large VSD causes a low blood oxygen level or to patients at highest risk of complications from infective endocarditis or Surgery.

• Surgeries.

Cardiopulmonary bypass in VSD surgeries replace heart and lungs function to provide a stable surgical field. Pulmonary Artery banding, is mostly done to critically ill infants with many VSDs or for those with associated complex cardiac malformations. Most perimembranous VSDs are repaired using a trans-atrial surgical method. VSDs in the outlet septum are approached through the pulmonary valve. Muscular VSDs, proximal to the apex, are complex to treat; hence, an approach through initial pulmonary banding through apical left ventriculotomy, to close the defect with a single patch is often used as a standard technique.

• Transcatheter closure

This approach may be used for multiple VSDs. The doctor inserts the catheter into a blood vessel and guides it to the heart, then uses a specially sized mesh device to close the hole. Muscular VSDs have been closed with transcatheter devices for ages now. Perimembranous VSDs, can be difficult to close percutaneously because of its proximity to the aortic valve resulting in potential aortic valve damage. The patient is often under general anesthesia and with transesophageal echocardiographic guidance during procedural closure. Reported complications have included aortic and tricuspid regurgitation, device embolization, transient left bundle-branch block, complete heart block, hemolysis, small residual shunts, and perforation.

Conclusion

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Based on the review of, Although VSD murmur is one of easier murmurs to recognize, sometimes an innocent physiological murmur can be mistaken for a VSD. Occasionally patent ductus arteriosus and pulmonary stenosis are mistaken for a Ventricular Septal Defect. Hence, it is imperative for clinicians to thoroughly understand the anatomy of congenital and acquired ventricular septal disease, and the ways they affect cardiovascular hemodynamics and performance. Diagnosis is subject to physical examination like auscultation to determine the presence of VSD; even such that are asymptomatic. Surgical and medical expertise is also essential and these help in the understanding and care of patients with cardiac malformations because these patients, can live productive lives when cared for appropriately.

References

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Prema Ramaswamy. (2015).Drugs & Diseases, Pediatrics: Cardiac Disease and Critical Care

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Wang, J., Zuo, J., Yu, S., Yi, D., Yang, X., Zhu, X., Yang, J. (2016). Effectiveness and safety

of transcatheter closure of perimembranous ventricular septal defects in adults. The American Journal of Cardiology, 117(6), 980-987. doi:10.1016/j.amjcard.2015.12.036

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Vibhuti N Singh. (2015). Drugs & Diseases, Radiology: Ventricular Septal Defect Imaging.

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Internal Medicine. Ventricular Septal Defects in Adults. Ann Intern Med. 2001;135:812-824. Retrieved from https://www.uthsc.edu/cardiology/articles/VSD%20review.pdf

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https://doi.org/10.1161/CIRCULATIONAHA.106.618124.Circulation. 2006;114:2190-2197

Originally published November 13, 2006

http://pediatricct.surgery.ucsf.edu/conditions–procedures/ventricular-septal-defect.aspx

http://circ.ahajournals.org/content/114/20/2190

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4569244/

https://en.wikipedia.org/wiki/Ventricular_septal_defect#Diagnosis

https://www.cincinnatichildrens.org/health/v/vsd

http://pubmedcentralcanada.ca/pmcc/articles/PMC2019978/pdf/archdisch01558-0006.pdf

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