Ventricular Septal Defect (VSD)

A hole connecting the 2 ventricles

Acyanotic

Left-Right Shunt

Causes

•          Congenital (prevalence 2:1000 births) à most common congenital cardiac malformation
•          Acquired (post-MI)

Type

1.       Membranous VSD (90%)

2.       Muscular VSD

3.       Single Ventricle

Clinical Feature

Small VSDs : asymptomatic & usually close spontaneously, with 90% no longer patent by 10 years of age

Moderate VSDs : Fatigue & SOB with cardiac enlargement & prominent apex beat.

                                 Palpable systolic thrill at lower left sternal edge & loud ‘tearing’ pansystolic murmur heard at the same position.

Large VSDs : cause pulmonary HPT (may lead to Eisenmenger’s syndromeà central cyanosis & finger clubbing)

** loud ‘tearing’ pansystolic murmur produced by flow from high pressure LV to low pressure RV during systole.It’s best heard at left sternal border.

On PE (auscultatory finding)

Small VSDs (‘maladie de Roger’) : Loud & sometimes Long Systolic Murmur

Moderate VSDs : loud ‘tearing’ pansystolic murmur

Large VSDs : cause pulomonary HPT & soft murmur

Cx

• AR
• IE
• Pulmonary HPT
•  Eisenmenger’s complex (In this condition, a ventricular septal defect (VSD) exists in conjunction with pulmonary vascular obstructive disease (PVOD). The resistance to blood flow to the lungs involved in PVOD causes a "right to left shunt" to occur, in which blood flows from the right ventricle into the left ventricle through the VSD)

Ix

§                             ECG

o   normal (small VSD)

o   LAD + LVH (moderate VSD)

o   LVH + RVH (large VSD)

§                           CXR

o   Normal heart size +- mild pulmonary plethora (small VSD)/ cardiomegaly

o   Large pulmonary arteries

o   Marked pulmonary plethora (large VSD)

Mx

1. Small VSD require no specific tx.only IE prophylaxis should be advised
2. Surgical repair of the defect
3. Cardiac failure should be treated with:

a.      Digoxin

b.      Frusemide

Tetralogy of Fallot’s

EPIDEMIOLOGY

Most common causes of cyanotic congenital heart disease

Most common CHD that survive (10%)

Four typical features of TOF

1. VSD

2. Pulmonary stenosis

3. Right ventricular hypertrophy

4. Aorta overriding VSD

CLINICAL FEATURES

Symptoms

            Dyspnoea and fatigue is main presentation

After exercise (hypoxic cell), child usually adopt a squatting position because it can increases peripheral vascular resistance and decreases the degree of Rt to Lt shunt.

Growth retarded

On CVS examination

            Central cyanosis (commonly present from birth)

            Clubbing of finger and toes + polycythaemia (obvious after 12 months)

            Auscultation : systolic ejection murmur at Lt upper sternal border

PATHOPHYSIOLOGY

With substantial obstruction of the Rt ventricular outflow tract, blood is shunted thru the ventricular septal defect from right to left. Thus the patient will presented with central cyanosis.

INVESTIGATION

CXR shows RV hypertrophy & small pulmonary artery (classic boot-shaped heart)

ECG shows RV hypertrophy with Rt bundle branch block (RBBB)

Echocardiography shows discontinuity between aorta and anterior wall of ventricular septum

CT & MRI give valuable information for planning the surgery

Boot-shaped heart

TREATMENTS

Without intervention (mortality rate 95% by age 20)

            Give 02 and place knee-chest position

            Morphine can sedate the child + relaxing the outflow of pulmonary

            Long term B-blocker may be needed

            Give endocarditis prophylaxis

With intervention ( survival rate is 90-95% by age 20)

In infants (palliative procedure usually done before age 1 yr) – an anastomosis  between subclavian artery and pulmonary artery (Blalock shunt), in order to increase blood supply to the lungs.  

Older child – A complete surgical correction is required.

REFERENCES
1.  Kumar P, Clark M, editors. Kumar and Clark Clinical Medicine, 7th ed.
2. Mohammad Inam Danish, editor. "Medical Diagnosis and Management"

3. Longmore,editor. “Oxford handbook of Clinical Medicine”

ATRIAL SEPTAL DEFECT

EPIDEMIOLOGY

·         Often diagnosis in adult

·         Women 3:1 Men

CLINICAL FEATURES

Symptoms

·              Asymptomatic for many years

·              Dysnoea, cardiac failure and atrial fibrillation are possible modes of presentation

On CVS examination

·              Mid-systolic ejection in pulmonary area

·              Loud P₂ , wide fixed splitting of S2

·              Diastolic flow murmur

PATHOPHYSIOLOGY

Communicating at level atria (interatrial septum) allows LEFT-to-RIGHT shunting of the blood. Because the pulmonary vascular resistance is low and the right ventricle easily distended, there is a considerable increase in right heart output. Murmur is produce by increase flow across pulmonary valve and increase stroke volume.

Above the age 30 years there may be an increase in pulmonary vascular resistance which can lead to pulmonary HPT. AF is common at this stage.

TYPES of ASD

1)Foramen secundum defect

     Commonest

-                   Excessive resorption of septum primum or inadequate development of septum secundum

2)Foramen primum defect:

-                   Septum primum fails to fuse with septum intermedium (endocardial cushion)

3)Sinus venosus defect:

-                  Incomplete absorption of the sinus venosus into right atrium

4)Common atrium

-                 The septum primum and secundum fail to develop

-                 The whole interatrial septum is absent.

INVESTIGATIONS

1.        1. Chest X-ray

     Prominent pulmonary artery
    Pulmonary plethora [fullness]
    Right ventricular hyperthrophy

2      2.  ECG

                     Usually shows some degree of RBBB due to right ventricle hyperthrophy

                     Right axis deviation

3      3. Enchocardiogram: shows RVH and pulmonary arterial dilatation

TREATMENT

Surgical repair of the large defect before the age of 10 years or as soon as possible if first diagnosed in adulthood.

REFERENCES
1.  Kumar P, Clark M, editors. Kumar and Clark Clinical Medicine, 7th ed.
2. Mohammad Inam Danish, editor. "Medical Diagnosis and Management"

Bismillah..

Assalammualaikum..
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