Ventricular Septal Defect

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Ventricular Septal Defect

The heart is a conical muscular organ. The main function of the heart is to regulate blood flow throughout the body by expanding and contracting caused by stimulation of the autonomic nervous system.

Congenital diseases are hereditary diseases that can occur from birth and some time after birth. VSD is a congenital heart disease in the form of a hole in the interventricular septum, there can be only one or several holes, which is due to a defect in the interventricular septum during intrauterine development of the fetus.

Ventricular septal defect - a congenital heart defect in the form of a hole between the left and right ventricle , only one or several holes due to a ventricular septal defect in the prenatal period, blood can flow from the left ventricle to the right or vice versa.

Picture. Ventricular septal defect. Blood from the left ventricle can flow directly into the right ventricle (Cardiac Point, 1997).

The abnormal condition is an opening between the left and right ventricles. A VSD is a defect that usually occurs in part of the membranous septum and is below the aortic valve. Sometimes the defect manifests itself in the muscle part.

Perimembranous VSDs can also be located under the annulus of the aortic or pulmonary valves, which is called a "double fixed VSD". VSDs are usually solitary but may be multiple, multiple muscle VSDs are referred to as "Swiss cheese VSDs".

VSD is a congenital (congenital) heart defect in the form of a hole in the interventricular septum, which determines the relationship of blood flow between the right and left ventricles. The opening usually closes by the end of the fourth week of pregnancy.

There may be only one or a few perforations caused by insufficient fusion of the interventricular septum during fetal development. VSD is the most common congenital anomaly, accounting for about 30.5%.

VSD classification by place of discovery, for example:

  1. Perimembranous (most common type, 60%), when the hole is located in the membranous part of the interventricular septum,
  2. subaero  Double hole, the valve is located in the region of the suprafundal septum, and the edge of the defect is formed by a tissue channel connecting the aortic valve and the pulmonary valve.
  3. The bilateral muscular opening is located in the region of the interventricular muscular septum.
A hole in the interventricular septum allows blood to flow from the left ventricle to the right ventricle due to a pressure gradient, which increases blood flow to the lungs. The clinical picture depends on the size of the defect and blood flow ( shunt ), as well as the size of the pulmonary vascular bed.

If the defect is small or limited, there are no symptoms (asymptomatic). Small left ventricular pressure gradient error > 64 mmHg Art., systolic pressure in the right ventricle and pulmonary resistance are normal.

with moderate defects with limited pressure gradients in the left and right ventricles of 36 mm Hg. Pulmonary resistance and right ventricular systolic pressure increase but do not exceed systemic pressure.

In this condition, the left ventricle and left atrium may become enlarged due to the increase in load volume. The right and left ventricles will have large uncontrolled defects characterized by the same systolic pressure, which will reduce blood flow from left to right and even from right to left.

In this situation, they experience ailments such as shortness of breath and fatigue, often coughing and recurrent respiratory infections. He is also huge dysplasia

At the same time, some VSDs may close spontaneously (perimembranous and muscular types), develop aortic valve prolapse with pulmonary hypertension, infundibular hypertrophy, or regurgitation (subarterial and perimembranous types) .

The exact reason is unknown. More than 90% of the causes of congenital heart defects are multifactorial. Damaging factors:

  1. External factors: various drugs, diseases of the parents (rubella, IDDM).
  2. Endogenous cause: genetic disease ( part of a specific syndrome ).
  3. Interaction of genetic and environmental factors.

The presence of ventricular defects increases the pressure in the left ventricle, and the resistance of the systemic arterial circulation is greater than the resistance of the pulmonary circulation. Blood drains through the septal defect into the pulmonary artery.

The volume of blood in the lungs increases and the pulmonary vascular resistance increases. At the same time, the pressure in the right ventricle increases due to the shunting of blood from left to right.

This will compromise endocarditis and cause right ventricular muscle atrophy, resulting in increased right atrial afterload, so that right atrial afterload does not increase and right atrial afterload increases. Overcoming resistance. Caused by incomplete emptying of the atria.

A VSD is characterized by the presence of a septal junction that allows blood to flow directly into the ventricles, usually from left to right. The defect diameter ranges from 0.5 to 3.0 cm.

About 20% of these defects in children are common defects, many of which close on their own. This defect is often combined with other heart defects. Physiological changes occur as follows:
  1. Left ventricular pressure remains high and increases the flow of oxygen-rich blood through the right ventricular defect.
  2. The increased volume of blood is pumped to the lungs, which fill with blood and can cause an increase in pulmonary vascular resistance.
  3. When this pulmonary resistance is high, pressure in the right ventricle increases, causing an oxygen-depleted outflow of blood from the right ventricle, resulting in cyanosis (Eisenmenger's syndrome).
Clinical manifestations
In both of these functions, the blood that enters the heart from the lungs is recirculated to the lungs. Blood production in the pulmonary veins increases and causes:

  1. He gets tired easily
  2. my rock
  3. Dikhavitsa is resting
  4. Slow weight gain and no weight gain
  5. Health while breastfeeding
  6. Excessive sweating.
The type of VVD can be determined by clinical signs:
1. Small VSD
  • usually asymptomatic
  • Normal or slightly enlarged heart and no growth and development abnormalities
  • normal pulse
  • An early short systolic murmur is detected before the initial systolic click.
  • There is also a pansystolic murmur. 

2. Average IRR

Symptoms that occur during breastfeeding include :

  • Shortness of breath when drinking or for a long time to finish eating.
  • Unsatisfactory weight gain
  • They often suffer from lung infections that take a long time to heal.  
  • He appears to be weakened with shortness of breath, discomfort, and withdrawal.
3. Large VSD
  • Frequent heart failure at 1-3 months of age
  • Often with lung infections
  • Gain weight gradually.
  • Dikhavitsa is resting
  • Sometimes there is cyanosis  
  • The trick is quite realistic  
  • Normal heart murmurs
  • A pansystolic murmur is heard
  • With or without vibration
  • Decreases at the end of systole

Physical examination reveals a holosystolic (pansystolic) tone heard in the systolic phase, loud in the tricuspid section of the left parasternal 3-4 intercostal space, rough, parasternal and spreading along the apex of the heart. This sound can be heard even with small VSD defects.

word Mid-diastole may be felt at the apex of the heart due to excess flow. VSDs are often not cyanotic unless enucleation occurs shunt from right to left). Patients with large VSDs with shunting flow have tachypnea, left ventricular hyperactivity, and systolic flutter.

When the flow comes shunt From right to left, with a large defect, stenosis will appear with stick fingers ( stick fingers ). With sufficiently large defects, complications such as external ossification stenosis, aortic valve prolapse, aortic insufficiency, pulmonary hypertension, and heart failure can occur.

A chest x-ray revealed cardiomegaly with involvement of the left ventricle. Vascularization of the lungs is increased, and when the pulmonary vessels are affected, a pruned tree (for example, unbranched) with a ledge is observed. Respiratory system.

An electrocardiogram may reveal left ventricular hypertrophy and possibly left atrial hypertrophy. In the presence of hypertrophy of both ventricles and deviation of the QRS axis to the right, pulmonary hypertension or hypertrophy of the trunk of the right ventricle is required.

With M-mode echocardiography, you can determine the size and position of the left ventricle, two atrial measurements, Doppler error and its color, as well as determine the direction and volume of blood flow through it. error

General checks:

1. Chest x-ray and ultrasound

2. The following pictures can be found on the ECG:

  • Normal (small VSD) 
  • HAki and HVki (medium and large VSD) 
  • HAki and HVleg (medium and large VSD) 
  • Pure HVCA (large VSD with persistent pulmonary hypertension).
  • Cardiac catheterization

The heart can be seen like this:
  • End systolic murmur just anterior to S2, left intercostal space at 3-4 inches per second.
  • Pansystolic murmur of the 3rd degree and higher on a 6-point scale, sharp, sharp in the left intercostal space.  
  • Pansystolic noise of 3-4 degrees on a 6-point scale, rough sharp sounds in the ribs for 3-4 hours. On the left, IPS grade 2/6 is a short low tone accompanied by a diastolic murmur at 4 o'clock. Left intercostal BCI.
  • Weak ejection-type systolic murmur, lower left evening Ips with S1 thickened, systolic click heard after S1 (opening of the pulmonic valve), S2 loud/very loud and solitary.  

5. Cardiac angiography
In radiology, you can find the following images:
  • The heart is normal with or without vasodilatation (small VSD). 
  • Cardiomegaly, trunk a. pulmonary edema with severe pulmonary edema and excessive vascular markings on the chest (medium and large VSD). 
  • Stem a. Large lungs (pronounced pulmonary edema), with branches a. Low pulmonary artery (large VSD with persistent pulmonary hypertension or Eisenmenger's syndrome).

medical management

  1. Vasopressors or vasodilators are drugs used in children with ventricular septal defects and severe chronic heart failure.
  2. Dopamine (intropin) has a positive inotropic effect on the myocardium, increases cardiac output and increases systolic and pulse pressure, has virtually no effect on diastolic pressure, is used to treat hemodynamic disorders due to open heart surgery (the dose is selected to maintain blood pressure). and renal perfusion).
  3. Isoproterenol (Isuprel) has a positive inotropic effect on the myocardium, resulting in an increase in cardiac output and heart function, a decrease in diastolic and mean pressure with an increase in systolic pressure.
Correction of a ventricular septal defect
Early repair is recommended if the defect is large. Patients with chronic heart failure may require total or palliative pulmonary artery ligation or fusion surgery if they cannot be clinically stabilized.

Because of the irreversible damage caused by pulmonary vascular disease, surgery should not be delayed for premature or progressive pulmonary vascular obstruction.

Some animals underwent median sternotomy and cardiopulmonary bypass by hypothermia. With a membrane defect at the top of the septum, an incision in the right atrium allows the surgeon to correct the defect by working through the tricuspid valve. Otherwise, a right or left ventriculotomy is required.

Usually a lavsan or pericardial patch is applied to the wound, although a straight suture may be used if the defect is minimal. The binding has been removed and all distortions have been corrected.

The surgical response should include a hemodynamically normal heart, although the damage caused by pulmonary hypertension is irreversible. The following complications of the disorder are possible:
1. The presence of aortic insufficiency (especially if it was present before surgery)
2. Arrhythmia

  • Blockade of the right leg of the bundle of His (right ventriculotomy)
  • Heart failure
3. Chronic heart failure, especially in children with pulmonary hypertension and left ventriculotomy.

5. Dis

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