this is one of (the synopses in GUCH) Series for general cardiologists that should acquire in GUCH

1. Ventricular septal defects
By
Dr.Aliaa Shaban
Lecturer of Cardiovascular Medicine
Synopses in ACHD

2. The scenario……………
• A 24-year-old lady with known ventricular septal defect since
childhood presented for evaluation of dyspnea on exertion,
fatigue, and atypical chest pain. No orthopnea, or edema.
• examination
• BP 120/70 mm Hg, HR 56 bpm. JVP : normal.
• The lungs were clear
• The cardiac examination
• no heave or thrill.
• Heart sounds : normal with no additional sounds.
• There was a grade 3/6 holosystolic murmur at the apex and
left sternal border with no diastolic murmur.
• no edema,NO clubbing, or cyanosis noted in the lower
extremities.
• Her electrocardiogram and chest x-ray, were unremarkable
with no definitive signs of left ventricular enlargement.

3. Anatomy

4. The ventricular septum can be divided into four
regions:
• membranous,
• inlet,
• outlet,
• trabecular

5. Inlet septum
• The inlet septum is
located between the
AV valves inferior to the
membranous septum
with its apical border
being the chordal
attachments of the AV
valves.

6. Outlet septum
• The outlet septum
makes up the most
anterior and superior
part of the ventricular
septum
• located above an
imaginary line between
the membranous
septum, and the
anterior infundibular
wall.

7. Trabecular septum
• The remainder of the ventricular
septum is the trabecular
septum, which is the largest region.
The trabecular septum is broken into
the sub regions :
o Posterior (sometimes called inlet
muscular),
o anterior,
o mid-muscular,
o apical.

8. o The posterior trabecular (or muscular) septum
is posterior to the septal attachment of the
tricuspid valve.
o The anterior trabecular septum is identified as
anterior to the mid-septum and at, or superior
to, the level of the moderator band.
o The mid-muscular septum is superior to the
moderator band.
o The apical septum is inferior to the moderator
band

10. Peri membranous VSD
• A defect in the IVS
adjacent to the
membranous portion of
the IVS and septal
leaflet of the TV.
• AV conduction tissue is
related to the posterior,
inferior aspect of the
defect.

11. • When the VSD extends primarily toward the
aortic valve, it is called a perimembranous
outlet defect;
• When the defect is primarily adjacent to the
tricuspid valve,it is called a perimembranous
inlet defect.

12. Synonyms of VSDs

13. Hemodynamics

14. The direction and severity of the left-to-right
shunt created by the VSD depends on:
• the functional size of the defect,
• systemic blood pressure,
• The presence of AR, DCRV, and pulmonary
hypertension.

15. Adult VSD hemodynamics
• EITHER:
1.Small restrictive defects. The PVR is not
significantly elevated and the left-to-right shunt is
small (Qp:Qs <1.5:1).
(Right ventricular systolic pressure is lower than the left
ventricular systolic pressure )
2. Large nonrestrictive defects in cyanotic patients
who have developed Eisenmenger syndrome, with
PVR at systemic levels and shunt reversal (right-to-
left).
(Pressures in both ventricles are balanced )
.

16. 3. Patients with moderately restrictive defects
(Qp:Qs ≥1.5:1 and <2:1) who have not
undergone closure at childhood.
(These patients often have mild-to-moderate
PAH.)
4. Patients who have had their defects closed in
childhood. These patients may have VSD
patch leaks

17. Aortic regurgitation (AR(
• AR due to prolapse of a coronary cusp
• This can result in reduction of functional size
of the defect and the left-to-right shunt, but
at the expense of aortic valve distortion, AR,
and further volume overload of the left
ventricle.

19. Double chamber right ventricle
DCRV
• Superior displacement of the (moderator
band) has been proposed, particularly in
association with a VSD, and flow turbulence in
the RVOT.
• This flow turbulence may trigger abnormal
hypertrophy of the moderator band leading to
DCRV.

20. PHT
• long-standing, unrestricted left-to-right shunt,
 the right ventricular pressure is at or near
systemic , minimal shunt across the VSD.
reversal of the shunt (cyanosis.)
• This right-to left shunting known as
Eisenmenger complex

21. Clinical presentation

22. • asymptomatic,
• new onset dyspnea or fatigue,
• endocarditis,
• syncope,
• Arrhythmias.
• Syncope is often exertional and can be due to
arrhythmias or significant right ventricular outflow
obstruction caused by a large prolapsing aortic valve
cusp, large aneurysm of membranous septum, or
DCRV.
• Patients can also present with a changing murmur; a
new murmur, such as the development of diastolic
murmur due to AR; or heart failure because of
progressive left ventricular volume overload and/or
pulmonary hypertension.

23. Cardiac Examination

25. Echocardiography

26. Peri membranous VSD
Views
• Parasternal long axis
• Parasternal short axis
• 4 ch view.
• Subcostal

32. peri membranous VSD& tricuspid
valve
• Because of their location adjacent to the
tricuspid valve, perimembranous
defects can be associated with tricuspid septal
leaflet distortion and tricuspid regurgitation.
• Accessory tissue from the septal leaflet of the
tricuspid valve, or a part of the septal leaflet
itself, can partially or completely close the
defect; this tissue is sometimes referred to as
a ventricular septal aneurysm .

35. Peri membranous VSD & Aortic valve
• As perimembranous VSDs are also adjacent to the
aortic valve, this valve can also be affected.
• In about 10% of perimembranous VSDs, there is
associated aortic valve prolapse, and in 6% to 8%,
there is associated aortic regurgitation.
• The right or non-coronary aortic cusp protruding into
the VSD.
• Because aortic cusp prolapse is more common with
subarterial defects, the presence or absence of aortic
cusp prolapse should be reported with any defect
located immediately adjacent to the aortic valve.

38. Muscular VSD
• Second most common type of VSD.
• Can be located anywhere in the muscular
septum, including: Anterior, posterior, mid,
and apical.
• • Multiple muscular VSDs may be referred to
as “Swisscheese” defects.

40. Anterior muscular VSD
• Anterior muscular defects extend along the
mid-septum from the insertion of the
moderator band toward the membranous
septum.

42. Mid muscular VSD
• Mid-muscular defects are anterior to the
septal attachment of the tricuspid valve, and
superior to the moderator band

46. Posterior muscular VSD
• Posterior muscular defects are located
posterior to the septal attachment of the
tricuspid valve; posterior-inlet muscular
defects are located immediately below AV
valves but separated from the valves by
muscle tissue.

47. Apical muscular VSD
• Apical muscular VSDs are located inferior to
the moderator band and include defects of
the RV inflow apex.

48. Sup pulmonic(supra cristal(
• Located inferior and anterior to the
pulmonary valve .
• Defects do not close spontaneously.
• Least common defect, representing 6% of
VSDs.
• Associated with aortic valve right cusp
prolapse with or without aortic regurgitation
(AR).

49. Sup pulmonic VSD
VIEWS
• Parasternal long axis view.
• Parasternal short axis view: at approximately
the 1 o’clock position with the jet aimed toward
the PA.
• Sub costal long axis and short axis views.

52. Inlet VSD
• Located posterior and superior in the inlet
septum beneath the septal leaflet of the TV.
• May involve malalignment of the IVS with
the atrial septum.
• Called: AV canal defect .

54. Inlet VSD
• Apical 4C
• Parasternal short axis
• Subcostal 4 ch
• Subcostal long axis
• Subcostal short axis view

56. steps
• 1-Type of the VSD
• 2-Size of the VSD
• 3-Direction of the shunt.
• 4-Complications
LV Volume overload
Pulmonary hypertension
(Hemo dynamically significant or not)

57. Hemodynamics

59. • The peak systolic velocity across it will reflect
the pressure gradient between the ventricles
at peak systole.
• Therefore:
RVSP = Systemic systolic BP − VSD max PG

60. QP/QS
• (CSARVOT
x VTIRVOT
)/(CSALVOT
x VTILVOT
).
• Cross sectional area (CSA) calculated from the
diameter of the right (RVOT) and left
ventricular outflow tract (LVOT) measured in
the 2D and velocity time integral (VTI) with
PW-Doppler .

62. Transesophageal
echocardiography
• is particularly useful in patients difficult to
visualize, to specify the relation of the defect
to other structures, e.g. to determine the
distance between the defect and the aortic
valve.

63. Cardiac MRI
• Cardiac MRI is particularly useful in adult
patients with a VSD and complex associated
lesions or with an inlet or apical VSD that
cannot be well seen by echocardiography.
• It may be indicated to quantify the severity of
aortic insufficiency and to assess left
ventricular size and function

64. Management

65. Indications of intervention:

67. Cardiac cath
• this may be performed to determine the
severity of PVR.
• trans cath closure .

68. Complication after VSD repair:
• Conduction defects, ( RT BBB in association with left anterior
hemiblock (especially after ventriculotomy and patch closure of
the defect.) Late sinus node dysfunction, including complete
heart block requiring pacemaker placement, is infrequent .
• Tachyarrhythmia, (increased pulmonary artery pressure.)
• Residual VSDs.
• Infective endocarditis, (in the presence of residual defect)
• Residual ventricular dysfunction (from long-standing volume
overload that could be aggravated by acquired CVD , such as
HTN and IHD)
• Residual AR .
• Tricuspid regurgitation due to septal leaflet distortion during
VSD repair.
• Residual pulmonary hypertension.

69. Pregnancy
• Pregnancy is well tolerated in women with
small or moderate VSD and in women with
repaired VSD.
• IE prophylaxis at the time of delivery is
indicated in patients with unrepaired VSD or
residual VSD patch leak.
• Pregnancy is contraindicated in patients with
VSD and the Eisenmenger syndrome

70. Exercise
• Patients with restrictive VSD do not require
exercise restrictions.
• • Patients with a moderate size VSD and some
degree of pulmonary hypertension
• should limit their exercise to low static and
low dynamic impact
• • Patients with VSD and Eisenmenger
physiology should not exercise