Ventricular Septal Defects: Drmlpatel Department of Medicine Kgmu

VENTRICULAR SEPTAL
DEFECTS
DR M L PATEL MD
DEPARTMENT OF MEDICINE
KGMU
OVERVIEW
• Introduction
• Definition
• Pathophysiology
• Types of VSD
• Clinical manifestation
• Diagnostic Tests
• Treatment
INTRODUCTION
• Ventricular septal defect is the most common form of congenital heart
disease and accounts for 15% to 20% of all such defects.
• It may occur in isolation or in association with other CHD like PDA and
coarctation of aorta.
• The functional disturbance depends on its size and on the status of the
pulmonary vascular bed.
• A wide spectrum exists in the natural history of VSD, ranging from
spontaneous closure to congestive cardiac failure and death in infancy.
DEFINITION
• It is defined as a congenital defect in the interventricular septum that leads to left
to right shunting of the blood.
NATURAL HISTORY-
• Natural history is mainly determined by the size of the defect and the status of
pulmonary vascular bed.
• Many VSDs (mostly small and muscular VSDs) undergo spontaneous closure in
childhood itself.
• Only small- or moderate-size VSDs are seen initially in adulthood, as most
patients with an isolated large VSD come to medical or surgical attention early in
life.
PATHOPHYSIOLOGY
MODERATE TO LARGE VSD
INCREASED BLOOD FLOW IN THE PULMONARY CIRCUIT
INCREASED BLOOD RETURN TO THE LV PULMONARY VASLCULAR

OBLITERATIVE CHANGES
LV VOLUME OVERLOAD INCREASED PULMONARY

VASCULAR RESISTANCE
LV DILATION AND CHF REVERSAL OF SHUNT/ EISENMENGER PHYSIOLOGY

PATHOLOGY: the ventricular septum
• The ventricular septum may be divided into a small membranous portion
and a large muscular portion.
• The muscular septum has three components:

• Inlet septum,
• Trabecular septum, and
• Outlet (infundibular or conal) septum.
• The trabecular septum (also simply called the muscular septum) is further
divided into anterior, posterior, mid, and apical portions.
ANATOMICAL CLASSIFICATION
• Perimembranous defects are most common (70%) , perimembranous
VSDs have been called perimembranous inlet (atrioventricular [AV] canal
type), perimembranous trabecular, or perimembranous outlet (tetralogy
type) defects.
• Outlet (infundibular or conal) defects account for 5% to 7% of all VSDs
• Inlet (or AV canal) defects account for 5% to 8% of all VSDs.
• Trabecular (or muscular) defects

CLASSIFICATION ON THE BASIS OF SIZE
• SMALL VSD - < 3 mm
• MEDIUM VSD – between 3- 6 mm
• LARGE VSD - > 6 mm
CLINICAL MANIFESTATION
SYMPTOMS
• With a small VSD, the patient is asymptomatic with normal growth and
development.
• With a moderate to large VSD, delayed growth and development, decreased

exercise tolerance, repeated pulmonary infections, and CHF are relatively
common during infancy.
• With long-standing pulmonary hypertension, a history of exertional dyspnea

and fatigue, chest pain, syncope and cyanosis is mostly present.
PHYSICAL EXAMINATION
• Before 2 or 3 months of age, infants with large VSDs may have poor
weight gain or show signs of CHF.
• Cyanosis and clubbing may be present in patients with pulmonary vascular
obstructive disease (Eisenmenger’s syndrome).
CARDIAC EXAMINATION -
• A systolic thrill may be present at the lower left sternal border.

• Precordial bulge and hyperactivity are present with a large-shunt VSD.
• The S2 is loud and single in patients with pulmonary hypertension or
pulmonary vascular obstructive disease.
• A grade 2 to 5 regurgitant systolic murmur is audible at the lower left
sternal border. It may be holosystolic or early systolic.
INVESTIGATIONS
Electrocardiography
• With a small VSD, the ECG findings are normal.
• With a moderate VSD, left ventricular hypertrophy (LVH) and occasional left
atrial hypertrophy (LAH) may be seen.
• With a large defect, the ECG shows biventricular hypertrophy (BVH) with or
without LAH.
• If pulmonary vascular obstructive disease develops, the ECG shows RVH only.
Radiography
• Cardiomegaly of varying degrees is present and involves the LA, left
ventricle (LV), and sometimes RV.
• Pulmonary vascular markings increase.

Echocardiography
• Two-dimensional and Doppler echocardiographic studies is the

investigation of choice.
• It can identify the number, size, and exact location of the defect;
• Estimate PA pressure;
• Identify other associated defects; and
• Estimate the magnitude of the shunt.

MANAGEMENT
Medical- is directed mainly to treat CHF. The main drugs used are-
• Diuretics- furosemide, torsemide, spironolactone.
• ACE inhibitors.
• Digoxin.
• In infants anemia, if present, should be corrected by oral iron therapy.
• Treatment of pulmonary infections with appropriate antibiotics.
• Supportive care
Surgical-
Indications and Timing:
• If growth failure cannot be improved by medical therapy, the VSD should be

operated on within the first 6 months of life, preferably by 3 to 4 months of age.
• Infants who have small VSDs and have reached the age of 6 months without
CHF or evidence of pulmonary hypertension are usually not candidates for
surgery.
• If the PA pressure is more than 50% of systemic pressure, surgical closure should
be done by the end of the first year.
• After 1 year of age, a significant left-to-right shunt with pulmonary to
systemic flow ratio (Qp/Qs) of at least 2:1 indicates that surgical closure is
needed, regardless of PA pressure.
• Surgery is not indicated for small VSD with Qp/Qs ratio less than 1.5:1.
• Older infants with large VSDs and evidence of elevated PVR should be
operated on as soon as possible.
Mortality-
• The surgical mortality rate is less than 1%.
• The mortality rate is higher for small infants younger than 2 months of
age, infants with associated defects, and infants with multiple VSDs.
Complications-
• RBBB and left anterior hemiblock
• Complete heart block.
• Residual shunt occurs in fewer than 5%.

Ventricular Septal Defects: Drmlpatel Department of Medicine Kgmu

Uploaded by

Copyright:

Available Formats

Ventricular Septal Defects: Drmlpatel Department of Medicine Kgmu

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Ventricular Septal Defects: Drmlpatel Department of Medicine Kgmu

Uploaded by

Copyright:

Available Formats

VENTRICULAR SEPTAL

INCREASED BLOOD FLOW IN THE PULMONARY CIRCUIT

INCREASED BLOOD RETURN TO THE LV PULMONARY VASLCULAR

LV VOLUME OVERLOAD INCREASED PULMONARY

LV DILATION AND CHF REVERSAL OF SHUNT/ EISENMENGER PHYSIOLOGY

• The muscular septum has three components:

• Trabecular septum, and

• Outlet (infundibular or conal) septum.

• Outlet (infundibular or conal) defects account for 5% to 7% of all VSDs

• Inlet (or AV canal) defects account for 5% to 8% of all VSDs.

• Trabecular (or muscular) defects

• With a moderate to large VSD, delayed growth and development, decreased

• With long-standing pulmonary hypertension, a history of exertional dyspnea

• A systolic thrill may be present at the lower left sternal border.

• Pulmonary vascular markings increase.

• Two-dimensional and Doppler echocardiographic studies is the

• Identify other associated defects; and

• Estimate the magnitude of the shunt.

• In infants anemia, if present, should be corrected by oral iron therapy.

• Treatment of pulmonary infections with appropriate antibiotics.

• If growth failure cannot be improved by medical therapy, the VSD should be

• The surgical mortality rate is less than 1%.

You might also like