Congenital heart disease

Congenital heart disease . It is used to describe disorders of the heart and great vessels that have existed before birth.Congenital heart disease or congenital heart disease refers to problems with the structure and function of the heart.


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  • 1 Classification of Congenital Heart Diseases
  • 2 Congenital Non-Cyanotic Heart Diseases
  • 3 Atrial septal defect
  • 4 Cyanotic Congenital Heart Injuries
  • 5 See also
  • 6 External link
  • 7 Source

Classification of Congenital Heart Diseases

1.Normal Lung Flow:

  1. Right ventricular hypertrophy:
  • Pulmonary stenosis.
  • Mitral stenosis
  1. Left ventricular hypertrophy:
  • Primary cardiomyopathy
  • Aortic stenosis.
  • Aortic coarctation.
  • Mitral regurgitation

2.Increased Pulmonary Flow:

  1. Right ventricular hypertrophy:
  • Ventricular septal defect
  • Atrial septal defect (secundum)
  • Patent ductus arteriosus
  1. Left ventricular hypertrophy (or combination):
  • Ventricular septal defect
  • Patent ductus arteriosus
  • Common ventricular atrium
  • Cyanotic Congenital Heart Diseases

3.Decreased Pulmonary Flow:

  1. Right ventricular hypertrophy:
  • Severe pulmonary stenosis with or without ventricular septal defect.
  • Pulmonary atresia with or without ventricular septal defect.
  • Tetralogy of Fallot.
  1. Left ventricular hypertrophy:
  • Tricuspid atresia
  • Pulmonary atresia with right ventricular hypoplasia.
  1. Right, left, or combined ventricular hypertrophy:
  • Transposition of great vessels with pulmonary stenosis.
  • Arterial trunk with hypoplastic pulmonary artery.

4.Increased Pulmonary Flow:

  1. Right ventricular hypertrophy:
  • Hypoplastic left ventricle syndrome
  • Transposition of great vessels.
  • Aortic atresia.
  • Totally abnormal pulmonary venous return.
  1. Right, left, or combined ventricular hypertrophy:
  • Transposition of great vessels
  • Tricuspid atresia with transposition of the great vessels
  • Single ventricle.

Non-Cyanotic Congenital Heart Diseases


Non-cyanotic congenital heart defects are classified according to the predominant physiological burden they create on the heart. The most frequent injuries are those that cause a volume overload and the most common among these are short circuits from left to right. Other causes of volume overload are regurgitation of the atrioventricular valve and some cardiomyopathies.

The second most common cause of congenital heart injury are those associated with pressure overload, usually secondary to obstruction of ventricular outflow (for example, aortic or pulmonary valve stenosis) or stenosis of one of the great vessels. (eg, aortic coarctation). X- ray and ECG are useful tools in differentiating the two main types of injuries due to pressure overload or volume.

  • Injuries Associated with Volume Overload.

The most frequent injuries in this group are those that produce short circuits from left to right, such as interatrial communication (CIA), ventricular septal defect (CIV), atrioventricular septal defect (AVC AV) and patent ductus arteriosus (CAP). The common denominator in the pathophysiology of this group is the communication between the systemic and pulmonary circulation, which results in a short circuit of completely oxygenated blood , which penetrates again into the Lungs .

  • Injuries Associated with Pressure Overload

The common denominator in the pathophysiology of these lesions is obstruction of normal blood flow. The most common obstructions are those that affect ventricular emptying, such as pulmonary valve stenosis, aortic valve stenosis, and aortic coarctation.

Ventricular filling obstructions are less frequent and include mitral or tricuspid stenosis and cor triatum. Ventricular emptying obstruction can occur at or below the valve (eg, right double-chamber ventricle or subaortic membrane) or above it (eg, pulmonary branch stenosis). or supravalvular aortic stenosis).

Cardiac output is maintained, unless the obstruction is severe, so that symptoms of heart failure are subtle or non-existent. This compensation implies an increase in wall thickness (hypertrophy).

Atrial septal defect

Interatrial Communications (CIA) can occur anywhere in the atrial septum (septum secundum, septum primum, or venous sinus). Rarely, the almost complete absence of the atrial septum occurs, resulting in a single atrium from a functional point of view. In contrast, the presence of a patent foramen ovale as an isolated finding generally lacks hemodynamic significance, and is therefore not considered a CIA.

However, if the right atrial pressure is elevated secondary to another heart condition (such as pulmonary stenosis or atresia, tricuspid valve abnormalities, or right ventricular dysfunction), the venous blood may short-circuit through the hole. oval patent to the left atrium, with the subsequent appearance of cyanosis.

Blood generally does not deviate from the left atrium to the right as a consequence of the anatomy of the patent foramen ovale. However, in the presence of significant volume overload or right atrial hypertension , or both, the dilatation of the foramen ovale may be sufficient to create a significant left-to-right shunt. The isolated presence of a patent oval hole does not require surgical treatment, but may pose a risk of systemic paradoxical embolization in adult life.

  • Ostium Secundum Inter-atrial Communication.

It is a defect in the interatrial septum, located in the region of the fossa ovalis; It is the most frequent type of CIA and is associated with the presence of normal atrioventricular valves. The defects can be single or multiple, and even in symptomatic older children it is possible to find holes 2 cm in diameter or larger. Large defects may extend downward to the Vena cava inferior and the orifice of the coronary sinus, or backwards. The female: male ratio is 3: 1.

  • Pathophysiology

The degree of short-circuit from left to right depends on the size of the defect, as well as the relative compliance of the right and left ventricles and relative vascular, pulmonary, and systemic resistances. Abundant blood flow through the right heart increases of atrium and ventricle size and pulmonary artery dilation.

Despite the significant magnitude of pulmonary flow, the pressure in the pulmonary artery is maintained, due to the lack of high-pressure communication between the pulmonary and systemic circulations. Pulmonary vascular resistance remains low during childhood , although it begins to rise in adulthood. The size of the left ventricle and aorta is normal.

  • Clinical manifestations

Children are generally asymptomatic, so the injury is discovered during an examination for other reasons. The pulses are normal. A systolic elevation of the right ventricle is usually palpable, from the left sternal border to the midclavicular line. The first cardiac tone is strong, and occasionally a popping lung sound is heard.

In most patients, the second cardiac tone, auscultated at the left superior sternal border, is widely unfolded, with a fixed unfolding in all phases of respiration.This finding of auscultation is characteristic and is due to the fact that the The defect produces a continuous elevation of the diastolic volume of the right ventricle, with a prolonged ejection time.

The systolic murmur is a medium-toned ejection murmur, without harsh timbres, rarely accompanied by thrill, and is optimally auscultated at the medial and superior left sternal border, due to increased flow through the right ventricular outflow path. into the pulmonary artery A brief, rumbling mesodiastolic murmur can usually be heard at the left inferior sternal border due to increased flow through the tricuspid valve.

  • Prognosis and Complications

CIA of the ostium secundum type is usually well tolerated during childhood; symptoms generally appear in or after the third decade of life. Late clinical manifestations are pulmonary hypertension, atrial arrhythmias, mitral or tricuspid regurgitation, and heart failure. These symptoms may appear for the first time during the volume overload situation that pregnancy brings. Infectious endocarditis is extremely rare. Postoperative complications, such as late heart failure and atrial fibrillation, are more frequent in patients who undergo surgery after the age of 20 years.

CIAs of the ostium secundum type are generally isolated lesions.

Cyanotic Congenital Heart Injuries

This group of congenital heart diseases can be divided in turn according to the pathophysiology, depending on whether there is a decrease in pulmonary vascular flow, as occurs in tetralogy of Fallot, pulmonary atresia with an intact septum, tricuspid atresia or pulmonary venous return. total anomalous with obstruction; or increased pulmonary flow, such as in transposition of the great vessels, single ventricle, truncus arteriosus, or abnormal total pulmonary venous return without obstruction. As with non-cyanotic lesions, chest radiography is a valuable tool for distinguishing between the two categories.

  • Cyanotic Lesions with Decreased Pulmonary Blood Flow

These injuries involve both an obstruction of the pulmonary blood flow (in the tricuspid valve, the right ventricle, or the pulmonary valve) and a pathway through which the Bloodsystemic venous is able to find a right-to-left shunt to reach systemic circulation (through the foramen ovale, a CIA, or a CIV). The most frequent injuries in this group include tricuspid atresia, tetralogy of Fallot, and various forms of single ventricle with pulmonary stenosis. In these lesions, the degree of cyanosis depends on the degree of obstruction of the pulmonary blood flow. If the obstruction is mild, there is sometimes no resting cyanosis. However, these patients can present hypercyanotic crises under stress conditions. Conversely, if the obstruction is severe, the pulmonary flow will depend on the patent ductus arteriosus. If the duct is closed during the first days of life, the newborn shows deep hypoxia and shock


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