Ventricular septal defect DR NIKUNJ .R .SHRKHADA (MBBS,MS GEN SURG DNB CTS SR)

1. VENTRICULAR SEPTAL DEFECT
BY DR NIKUNJ
(CTS RESIDENT STAR HOSPITAL)
(Coordinator:DR P.SATYENDRANATH PATHURI)
(8/4/19)

2. VENTRICULAR SEPTAL DEFECT
• A ventricular septal defect (VSD) is a hole between the left and right ventricles.
• A VSD may occur as an isolated anomaly or with a wide variety of intracardiac
anomalies.
• Banding of the pulmonary artery as a palliative maneuver was first described in
1952.
• Until the mid-1960s when primary VSD closure became safer, pulmonary artery
banding was the procedure of choice in managing VSDs. The first VSD closure was
performed in 1955 by Lillehei and associates at the University of Minnesota,
usingcontrolled cross-circulation between the child and parent. Nineteen of the 27
patients who underwent this procedure survived.
• In 1957, Kirklin and associates at the Mayo Clinic closed a VSD using a heart-lung
machine. In 1957, transatrial VSD closure was performed,4 followed in 1971 by the
popularization of primary repair in symptomatic infants by Barratt-Boyes and
associates using cardiopulmonary bypass, deep hypothermia, and circulatory
arrest.

3. ANATOMY OF THE TRICUSPID VALVE, RIGHT VENTRICULAR
SEPTUM, AND CONDUCTION SYSTEM
• The tricuspid valve has three leaflets: anterior, septal, and posterior.
• The anterior leaflet is connected via the chordae tendineae cordis to the anterior papillary
muscle (located on the anterior right ventricular free wall) and to the septal papillary muscle
(sometimes called muscle of Lancisi).
• The septal papillary muscle is itself part of the septal band of the septomarginal trabecula.
• The posterior leaflet is attached to the anterior and posterior papillary muscles, and the
septal leaflet attaches to the posterior and septal papillary muscles.

4. RIGHT ATRIAL CAVITY

8. • The right ventricular septum has five components
• 1. The membranous septum
• 2. The atrioventricular (AV) canal or inlet septum
• 3. The muscular septum (apical trabecular septum or sinus septum)
• 4. The trabecula septomarginalis (septal band and moderator band)
• 5. The conal septum (infundibular septum and parietal band

9. • Unlike the left ventricular septum, which is free of any papillary muscle attachment (the
mitral valve can be called “septophobic,” whereas the tricuspid valve can be called
“septophilic”), the right ventricular septum is where the septal (sometimes called medial)
papillary muscle and part of the posterior papillary muscle originate.
• The membranous septum is the only fibrous component of the septum. It is wedged between
the aortic valve, the tricuspid valve, and the mitral valve. Because the tricuspid valve is
normally apically displaced vis-à-vis the mitral valve, a portion of membranous septum ends
up between the right atrium and the left ventricle, called the AV part of the membranous
septum.
• The portion of membranous septum located between both ventricles is called the
interventricular part.

11. CONDUCTION SYSTEM
• The various atrial conduction tracts all converge toward the AV node . The AV node is located
in the inferior-posterior portion of the membranous septum, just inferior to the anteroseptal
commissure of the tricuspid valve.
• A different description of its location is that it occupies the apex of the triangle of Koch,
which is limited by the ligament of Todaro posteriorly, the orifice of the coronary sinus
inferiorly, and the tricuspid valve annulus superiorly.
• From the AV node, the common AV bundle of His descends within the interventricular part of
the membranous septum (or, in the case of a membranous VSD, the posteroinferior rim of
the VSD), traverses the septum, and then courses along the left ventricular aspect of the
septum
• It then separates into a right bundle branch, which travels back to the right ventricular
surface, as well as a left bundle branch.
• At the anteroinferior border at the level of the muscle of Lancisi, the right bundle branch
descends toward the right ventricular apex.

14. ANATOMIC CLASSIFICATION OF VENTRICULAR SEPTAL DEFECTS
• A useful surgical classification of VSDs was
initially developed in 1980 by Soto and
associates

15. ANATOMIC CLASSIFICATION OF VENTRICULAR SEPTAL DEFECTS
•further modified by Van Praagh and associates

17. • VSDs can be classified as follows:
• Conoventricular (or membranous) defects
• Conal (or outlet) VSDs
• Inlet (or AV canal type) VSDs
• Muscular VSDs (single or multiple)

19. CONOVENTRICULAR (OR MEMBRANOUS) DEFECTS
• located between the conal septum and the ventricular septum.
• They are centered around the membranous septum
• comprise 80% of all VSDs.
• They may be located exclusively in the membranous septum, or they can extend beyond the
boundaries of the membranous septum in the inferior, posterior, or anterior direction and
are then sometimes called perimembranous or paramembranous VSDs.
• Neither perimembranous nor paramembranous correctly describes the typical defect
involving the membranous septum and extending into the adjacent septum.
• The current recommendation is to call these defects either membranous VSDs or
conoventricular defects.

20. • Malalignment of the conal septal plane vis-à-vis the ventricular septal plane results in the
typical conoventricular defect.
• The malalignment can be anterior, as seen in tetralogy of Fallot, for example, or posterior, as
seen in interrupted aortic arch.
• In addition to resulting in a VSD, anterior conal septal malalignment also results in right
ventricular outflow tract obstruction, whereas posterior malalignment of the conal septum
results in left ventricular outflow tract obstruction
• When the ventricular portion of the membranous septum is entirely absent, the VSD extends
to the base of the aortic valve (sometimes called subaortic VSD).

21. CONAL VENTRICULAR SEPTAL DEFECTS
• Approximately 8% of VSDs are located in the conal (infundibulum or outlet) septum. They
also are called supracristal VSDs.
• They are either entirely surrounded by muscle (muscular conal VSDs) or limited upstream by
the aortic or pulmonary annuli (sometimes called subarterial VSDs)

22. INLET (OR ATRIOVENTRICULAR CANAL TYPE) VENTRICULAR
SEPTAL DEFECTS
• Inlet VSDs are characterized by the absence of part or all of the AV canal (inlet) septum.
• These VSDs are located immediately underneath the septal leaflet of the tricuspid valve, with
no tissue in between.
• Approximately 6% of all VSDs are inlet-type VSDs

23. MUSCULAR VENTRICULAR SEPTAL DEFECTS.
• Muscular VSDs (10% of all VSDs) are entirely surrounded by muscle.
• They can occur anywhere in the trabecular portion of the septum and can be isolated or
multiple.
• They are described by their location—that is, anterior, midventricular (between the muscular
septum and the septal band), posterior, or apical. When inspected through the left side of
the septum, what appeared to be multiple muscular defects often converge into either a
single hole or two separate holes

24. SEQUELAE OF LEFT-TO-RIGHT SHUNTING
• Left-to-right shunting at the ventricular level implies increased pulmonary blood flow.
• Therefore, left ventricular preload is similarly increased, resulting in increased workload for
both left and right ventricles.
• The left atrium is enlarged, and the left atrial pressure is elevated.
• The left ventricle dilates.
• The raised left atrial pressure causes many infants with VSD to have an increased
accumulation of interstitial fluid in the lungs, resulting sometimes in repeated pulmonary
infections.
• The work of breathing is increased as the lung compliance is decreased.
• This increases energy expenditure, which, along with the relatively low systemic blood flow,
causes these infants to have striking failure to thrive.

25. • When pulmonary resistance rises as a result of the development of pulmonary vascular
disease, pulmonary blood flow is reduced and the child appears to improve.
• Unfortunately, further increases in PVR occur, and the classic Eisenmenger complex results.
• These patients are characterized by fixed pulmonary hypertension, bidirectional shunting,
right ventricular hypertrophy, and a normal-sized left ventricle. They are often inoperable and
require heart-lung transplantation for further survival.

26. SHUNT DIRECTION AND MAGNITUDE
• Large VSDs offer little or no resistance to blood flow and are therefore called nonrestrictive.
The right ventricular pressure equals the left ventricular pressure, and the ratio of pulmonary
to systemic flow (Qp/Qs) (or shunt) is dependent on the ratio of pulmonary vascular
resistance (PVR) to systemic vascular resistance (SVR).
• On the other hand, small VSDs offer resistance to flow across the defect and are therefore
termed restrictive VSDs. The Qp/Qs rarely exceeds 1.5.
• Moderate-sized VSDs fall between these two categories and the Qp/Qs usually ranges
between 2.5 and 3.

27. NATURAL HISTORY

28. NATURAL HISTORY AND INDICATIONS FOR SURGERY
• Approximately 30% of infants with severe symptoms such as intractable congestive heart
failure or failure to thrive require surgery within the first year of life.
• The remainder can usually be managed medically, because the natural history of VSDs is well
known.
• Aggressive medical management is indicated because most membranous and muscular VSDs
tend to close spontaneously.
• Malalignment conoventricular VSDs or inlet-type VSDs are unlikely to close spontaneously,
and therefore closure at the time of diagnosis is recommended, regardless of age or weight.
• Asymptomatic children with isolated small restrictive VSDs can be followed safely with serial
echocardiograms.

29. • cardiac catheterization and measurement of PVR-to-SVR ratio should help with
decision making.
• In addition, pulmonary artery (PA) pressures greater than one half the systemic
pressure in a child older than 1 year indicate the need for surgery.
• If PA pressures are greater than one half the systemic, the response of the
pulmonary vasculature to inhaled nitric oxide and 100% inspired oxygen should be
studied during catheterization.
• Even children who have significant pulmonary hypertension with a reversible
component to it can become operative candidates.

30. • During the first decade of life, a small proportion (5%) of patients with membranous or outlet
VSDs develop prolapse of an aortic cusp into the VSD.
• This usually results in a gradual decrease of the effective orifice and shunt flow and also in
increasing aortic regurgitation.
• Increasing aortic cusp prolapse and regurgitation are an indication to operate.

31. PULMONARY VASCULAR DISEASE
• The classic description of the pathology of hypertensive pulmonary vascular disease is that of
Heath and Edwards.
• They correlated the PVR of patients with large VSDs with the histologic severity of pulmonary
vascular changes

33. • It is assumed that Heath-Edwards grade 3 or greater is not reversible.
• The importance of lung biopsies has decreased over the years, with catheterization-based
data increasing in importance in terms of suitability for repair

34. DIAGNOSIS
• Results of the physical examination, chest radiograph, and electrocardiogram (ECG) depend
on the underlying pathophysiology.
• Patients with large VSDs and increased pulmonary blood flow usually have symptoms such as
tachypnea, growth failure, profuse sweating during feeding, a bulging precordium, a
pansystolic murmur, an enlarged liver, and thready pulses.
• ECG shows signs of biven- tricular enlargement.
• In contrast, patients with small VSDs and small left-to-right shunts have only a systolic
murmur.
• The chest radiograph and ECG may be entirely normal. Two-dimensional echocardiography
and color flow Doppler studies have essentially replaced cardiac catheterization in most
patients with isolated VSDs. Cardiac catheterization is needed only when PVR and PA
pressure need to be measured.

35. The chest film shows a large central and peripheral PA and enlarged left atrium and ventricles