Congenital Heart Defects: Overview and Practice Questions

Congenital heart defects are among the most common birth anomalies, affecting the structure and function of the heart from birth. These defects range in severity from minor issues that may require no treatment to complex abnormalities that can significantly impact a person’s health and quality of life.

Understanding congenital heart defects is essential for both early detection and effective management, as advances in medical care have made it possible for many individuals with these conditions to live longer, healthier lives.

This article provides an overview of congenital heart defects, exploring their types, causes, symptoms, and treatment options.

What are Congenital Heart Defects?

Congenital heart defects are structural abnormalities of the heart that are present at birth. These defects can affect the heart’s walls, valves, or blood vessels, disrupting normal blood flow and heart function.

They vary widely in severity—from simple issues that may not require treatment to complex defects that need immediate intervention or surgery. The defects can cause symptoms such as difficulty breathing, fatigue, or poor growth in infants.

While the exact cause of congenital heart defects is often unknown, factors such as genetics, maternal health, and environmental influences can play a role. Early diagnosis and modern treatments have greatly improved outcomes for those with heart defects.

Types of Congenital Heart Defects

There are various types of congenital heart defects, each affecting the heart’s structure and function differently.

Here are some of the most common types:

• Tetralogy of fallot
• Transposition of the great arteries
• Aortic valve stenosis
• Coarctation of the aorta
• Ebstein anomaly
• Patent ductus arteriosus
• Pulmonary valve stenosis
• Atrial septal defect
• Ventricular septal defect
• Hypoplastic left heart syndrome
• Tricuspid atresia
• Truncus arteriosus
• Pulmonary atresia
• Single ventricle defect
• Total anomalous pulmonary venous return

Watch this video or keep reading to learn more about the most common types of congenital heart defects and how they impact heart function and overall health.

Tetralogy of Fallot

Tetralogy of Fallot is a complex congenital heart defect composed of four different abnormalities: a ventricular septal defect (a hole between the heart’s lower chambers), pulmonary stenosis (narrowing of the pulmonary valve), an overriding aorta (where the aorta is positioned over the ventricular septal defect), and right ventricular hypertrophy (thickening of the right ventricular muscle).

This condition reduces the flow of oxygenated blood to the body, often causing cyanosis, a bluish tint to the skin, especially noticeable during physical exertion. Surgical intervention is typically required to correct these abnormalities and improve oxygen flow.

Transposition of the Great Arteries

Transposition of the great arteries is a serious condition in which the two main arteries leaving the heart—the pulmonary artery and the aorta—are reversed. This causes oxygen-poor blood to circulate through the body while oxygen-rich blood recycles back to the lungs, resulting in low oxygen levels in the bloodstream.

Immediate medical intervention, often followed by surgical correction, is essential to ensure proper blood flow and oxygenation in the body. TGA is typically identified soon after birth due to severe cyanosis and other symptoms.

Aortic Valve Stenosis

Aortic valve stenosis is a condition where the aortic valve, which controls blood flow from the heart to the aorta and onward to the rest of the body, is narrowed. This restricts blood flow, causing the heart to work harder to pump blood through the narrowed opening.

Over time, this increased workload can lead to heart muscle thickening, fatigue, chest pain, and, in severe cases, heart failure. Treatment may involve monitoring, medication, or surgical intervention, such as valve repair or replacement, depending on the severity.

Coarctation of the Aorta

Coarctation of the aorta is a congenital defect characterized by a narrowing of the aorta, the major artery that delivers blood from the heart to the body. This narrowing can lead to high blood pressure, reduced blood flow to the lower body, and increased strain on the heart.

Symptoms vary based on the severity of the narrowing and may include hypertension, shortness of breath, and fatigue. Treatment often involves surgical correction or balloon angioplasty to widen the narrowed section and improve blood flow.

Ebstein Anomaly

Ebstein anomaly is a rare heart defect in which the tricuspid valve—the valve separating the right atrium from the right ventricle—is malformed and positioned lower than normal in the right ventricle. This can lead to poor valve function and backward blood flow, causing the right atrium to enlarge and reducing the heart’s ability to pump effectively.

Symptoms vary but may include cyanosis, fatigue, and heart palpitations. Treatment depends on the severity and can range from medication to surgical repair or valve replacement.

Patent Ductus Arteriosus

Patent ductus arteriosus (PDA) is a condition where the ductus arteriosus, a blood vessel that allows blood to bypass the lungs in a fetus, fails to close after birth. This results in abnormal blood flow between the aorta and pulmonary artery.

If left untreated, PDA can lead to respiratory problems and heart failure over time. Mild cases may close on their own, while larger PDAs typically require medical intervention, such as medication or a catheter-based procedure, to close the vessel and restore normal circulation.

Pulmonary Valve Stenosis

Pulmonary valve stenosis is a condition where the pulmonary valve, which regulates blood flow from the right ventricle to the lungs, is narrowed. This narrowing restricts blood flow to the lungs, forcing the right ventricle to work harder to pump blood through the valve.

Symptoms can vary, from mild fatigue and shortness of breath to severe cases where heart failure may occur. Treatment options depend on severity and may include balloon valvuloplasty to widen the valve or surgical repair.

Atrial Septal Defect

An atrial septal defect is a hole in the wall (septum) that separates the heart’s two upper chambers (atria). This defect allows oxygen-rich blood to mix with oxygen-poor blood, which can increase the workload on the heart and lead to complications like arrhythmias, pulmonary hypertension, and heart failure if untreated.

Some small atrial septal defects may close on their own, but larger ones typically require surgical repair or closure with a catheter-based procedure.

Ventricular Septal Defect

Ventricular septal defect (VSD) is a hole in the wall (septum) between the heart’s two lower chambers (ventricles). This opening allows oxygenated blood to mix with deoxygenated blood, causing the heart to work harder to supply the body with sufficient oxygen.

Symptoms can range from mild to severe, depending on the size of the defect, and may include difficulty breathing, fatigue, and poor weight gain in infants. Small VSDs may close on their own, while larger ones often require surgical repair to prevent long-term complications.

Hypoplastic Left Heart Syndrome

Hypoplastic left heart syndrome (HLHS) is a severe congenital defect in which the left side of the heart is underdeveloped, impacting the heart’s ability to pump oxygenated blood to the body. This defect affects multiple structures on the left side of the heart, including the left ventricle, aorta, and mitral valve.

HLHS is typically detected soon after birth, as it causes severe cyanosis and life-threatening symptoms. Treatment requires a series of surgeries or, in some cases, a heart transplant to help the heart function effectively.

Tricuspid Atresia

Tricuspid atresia is a condition where the tricuspid valve, which regulates blood flow between the right atrium and right ventricle, is absent. As a result, blood cannot flow normally from the right atrium to the right ventricle, leading to poor oxygenation.

The body compensates by creating alternate pathways, but these can cause strain on the heart and lead to complications. Symptoms often include cyanosis, difficulty breathing, and fatigue. Treatment usually involves surgery to create a functional pathway for blood flow and improve oxygenation.

Truncus Arteriosus

Truncus arteriosus is a rare congenital heart defect in which a single blood vessel arises from the heart, rather than separate pulmonary and aortic arteries. This causes oxygen-rich and oxygen-poor blood to mix and reduces the efficiency of oxygen delivery to the body.

Infants with truncus arteriosus often present with symptoms like cyanosis, difficulty breathing, and poor feeding. Surgical correction is necessary to separate the blood flow pathways and create proper circulation, typically within the first few months of life.

Pulmonary Atresia

Pulmonary atresia is a defect where the pulmonary valve, which connects the right ventricle to the lungs, does not form properly, blocking blood flow from the right ventricle to the lungs. This leads to inadequate oxygenation, as blood cannot easily reach the lungs for oxygen.

Infants with this condition may exhibit cyanosis and other severe symptoms shortly after birth. Treatment typically involves a combination of medications, catheter-based interventions, and surgery to create an alternative pathway for blood flow to the lungs.

Single Ventricle Defect

A single ventricle defect is a broad term for conditions where only one of the heart’s ventricles is fully functional. This defect impairs the heart’s ability to pump blood efficiently, as it must rely on a single ventricle to manage the workload normally divided between two.

Symptoms vary but often include cyanosis, difficulty feeding, and fatigue. Treatment usually requires a series of surgeries to reconfigure blood flow pathways, enabling the single ventricle to effectively circulate blood to both the body and the lungs.

Total Anomalous Pulmonary Venous Return

Total anomalous pulmonary venous return is a condition where the pulmonary veins, which should carry oxygen-rich blood from the lungs to the left atrium, instead connect to the right side of the heart. This leads to a mixture of oxygen-poor and oxygen-rich blood, decreasing the efficiency of oxygen delivery to the body.

Symptoms typically appear shortly after birth and can include cyanosis and difficulty breathing. Surgical correction is necessary to reroute the pulmonary veins to the left atrium, restoring normal blood flow.

Congenital Heart Defect Practice Questions

1. What affects pulmonary vascular resistance?
Pulmonary vascular resistance is affected by changes in PaO2, PaCO2, and pH levels.

2. What are the two categories commonly used to classify congenital cardiac defects?
Congenital cardiac defects are typically classified as cyanotic or acyanotic.

3. The patent ductus arteriosus connects which two vessels?
It connects the aorta to the pulmonary artery.

4. What is the therapeutic goal of subambient oxygen therapy?
The goal is to increase pulmonary vascular resistance.

5. The purpose of managing pulmonary vascular resistance in the presence of cardiac defects is to ensure what desired balance?
To maintain a balance between systemic and pulmonary blood flow.

6. Tetralogy of Fallot consists of which 4 associated conditions?
Right ventricular hypertrophy, overriding aorta, pulmonary stenosis, and ventricular septal defect.

7. Increasing gradients between ETCO2 and PaCO2 in patients with congenital cardiac defects are often the result of what?
Ventilation/perfusion (V/Q) mismatching.

8. What does the normal human heart contain?
The heart has 4 chambers: 2 atria and 2 ventricles.

9. What connects the atria to the ventricles?
The atrioventricular (AV) valves connect the atria to the ventricles.

10. Each ventricle’s outflow contains a valve called what?
Each outflow has a semilunar valve.

11. What is the function of the semilunar valve?
The semilunar valve allows blood to flow in only one direction, preventing backflow.

12. Where does blood flow begin with deoxygenated venous blood?
Deoxygenated blood enters the right atrium from one of three sources.

13. How does venous blood enter the right atrium?
Venous blood from organs above the heart enters via the superior vena cava, from organs below the heart via the inferior vena cava, and from the heart itself via the coronary sinus.

14. Where does blood travel from the right atrium?
Blood travels through the right AV valve (tricuspid valve) into the right ventricle.

15. From the right ventricle, blood flows through which valve?
It flows through the right semilunar valve (pulmonary valve) into the main pulmonary artery.

16. What are the divisions of the main pulmonary artery?
The main pulmonary artery divides into the right and left pulmonary arteries, carrying blood to the lungs.

17. What occurs in the lungs?
The lungs are the primary site of gas exchange.

18. Where is CO2 diffused in the lungs?
CO2 diffuses out of the blood and into the lungs for exhalation.

19. Where is oxygen diffused in the lungs?
Oxygen diffuses from the lungs into the blood.

20. How does oxygenated blood return to the heart?
Oxygenated blood returns via the four pulmonary veins, which empty into the left atrium.

21. From the left atrium, blood flows through what?
It flows through the mitral valve into the left ventricle.

22. Lastly, blood is pumped out of the left ventricle through what?
It is pumped through the left semilunar valve (aortic valve) into the aorta.

23. What is the aorta?
The aorta is the main vessel supplying systemic blood flow to the body.

24. What are the 3 fetal shunts?
The ductus venosus (controls blood flow from the placenta to the liver), the foramen ovale (between the right and left atria), and the ductus arteriosus (connects the pulmonary artery to the aorta).

25. How does the fetus perform gas exchange during development?
During fetal development, gas exchange is dependent on the mother’s lungs, as the fetus receives oxygenated blood through the placenta.

26. What happens when the lungs inflate and gas exchange begins?
As the lungs inflate, PaO2 levels increase, and PaCO2 levels decrease, which contributes to the dilation of pulmonary vasculature and a reduction in pulmonary vascular resistance (PVR).

27. A reduction in PVR leads to what?
It leads to decreased right ventricular pressures and increased pulmonary blood flow.

28. When does right atrial pressure decrease?
Right atrial pressure decreases when the umbilical cord is clamped, stopping placental blood flow to the inferior vena cava (IVC).

29. Why does the foramen ovale close?
The foramen ovale closes due to higher left atrial pressure and lower right atrial pressure.

30. When and why does the ductus arteriosus close?
The ductus arteriosus typically closes within 48 hours after birth due to increased oxygenation and decreased circulating prostaglandin E2 levels.

31. What is left-to-right shunting?
Left-to-right shunting occurs when oxygenated blood from the left heart or aorta flows into the right heart or pulmonary artery, mixing with deoxygenated blood.

32. What is Patent Ductus Arteriosus (PDA)?
PDA is a common congenital defect in the NICU. It can lead to left atrial dilation, left ventricular volume overload, and congestive heart failure (CHF). A preductal/postductal PaO2 difference >15 mmHg or SpO2 difference >5% suggests PDA.

33. What is an Atrial Septal Defect (ASD)?
ASD is a defect that causes right atrial enlargement, right ventricular volume overload, and increased pulmonary blood flow, potentially leading to an enlarged right ventricle, CHF, and pulmonary vascular disease.

34. What are the three types of ASD?
The three types of ASD are Ostium Secundum (most common and easiest to repair), Sinus Venosus, and Ostium Primum. Surgery is typically delayed until age 3-5 and may close spontaneously.

35. What is a Ventricular Septal Defect (VSD)?
VSD is a defect that may lead to left ventricular volume overload, left atrial enlargement, and increased pulmonary blood flow. It may decrease in size over time but does not enlarge.

36. What is an Atrioventricular Septal Defect?
Also known as an atrioventricular canal or endocardial cushion defect, this is the absence of septa between the atria and ventricles, commonly found in infants with Down syndrome.

37. What is aortic stenosis?
Aortic stenosis can occur in three forms: subvalvular (a ring around the valve), valvular (the valve itself, most common), and supravalvular (above the valve).

38. What is coarctation of the aorta?
Coarctation of the aorta is severe narrowing of the thoracic aorta near the ductus arteriosus, increasing afterload on the left ventricle, which can lead to increased wall tension and myocardial work. Systemic blood flow may be ductal-dependent.

39. What is pulmonic stenosis?
Pulmonic stenosis is a fixed obstruction of blood flow from the right ventricle to the pulmonary artery, often involving the pulmonary valve or artery itself. Moderate to severe stenosis can lead to right heart failure.

40. What is Hypoplastic Left Heart Syndrome (HLHS)?
In HLHS, systemic blood flow is maintained by pulmonary venous blood flowing through the foramen ovale to the right atrium. Requirements include a non-restrictive atrial septal connection, functional right ventricle, patent ductus arteriosus (PDA), and balanced pulmonary and systemic circulation. Prostaglandin E1 is used to keep the PDA open, and sub-ambient oxygen (17-21% FiO2) is used to increase PVR, with a target SpO2 of 70-80%.

41. What are cyanotic congenital heart lesions?
These are heart defects where deoxygenated blood is shunted to the left side of the heart, reducing systemic oxygen saturation.

42. What would be seen on a chest X-ray in Tetralogy of Fallot?
A chest X-ray in Tetralogy of Fallot typically shows a “boot-shaped” heart appearance.

43. What is Tetralogy of Fallot?
Tetralogy of Fallot is a common congenital heart defect with four components: pulmonary stenosis, ventricular septal defect, overriding aorta, and right ventricular hypertrophy. It may be ductal-dependent if pulmonary stenosis is severe.

44. What is truncus arteriosus?
In truncus arteriosus, a single arterial trunk arises from the heart, supplying systemic, pulmonary, and coronary circulation. A large VSD allows complete mixing of oxygenated and deoxygenated blood, with a target SpO2 in the 70s.

45. What does transposition of the great arteries show on a chest X-ray?
Transposition of the great arteries typically shows an “egg on a string” appearance on a chest X-ray.

46. What is transposition of the great arteries?
This condition involves the reversal of the aorta and pulmonary artery positions. The aorta arises from the right ventricle, while the pulmonary artery arises from the left ventricle, resulting in separated oxygenated and deoxygenated blood flows. Survival relies on mixing through ASD, VSD, or PDA.

47. What is pulmonary atresia?
In pulmonary atresia, blood flow from the right ventricle is obstructed due to atresia of the pulmonary valve. Blood reaches the left side of the heart via ASD or patent foramen ovale (PFO). Pulmonary blood flow is ductal-dependent, with a target SpO2 of 75%.

48. What does positive pressure ventilation do?
Positive pressure ventilation increases intrathoracic pressure, which can decrease systemic venous return to the right atrium.

49. How does increased intrathoracic pressure affect cardiac output?
Higher intrathoracic pressures from positive pressure ventilation may decrease cardiac output.

50. What is the “Tet spell” in Tetralogy of Fallot, and how can it be managed?
A “Tet spell” is a sudden episode of cyanosis due to a drop in oxygen levels, often triggered by crying or feeding. It can be managed by placing the child in a knee-chest position, which increases systemic vascular resistance and helps redirect blood flow to the lungs.

51. What is a ventricular septal defect (VSD) and what is it associated with?
VSD is a defect in the ventricular septum, resulting in a left-to-right shunt. Severity depends on the size of the defect. It is the most common congenital heart defect and is associated with fetal alcohol syndrome.

52. How is a ventricular septal defect treated?
Treatment often involves surgical closure, although small defects may close spontaneously.

53. What is an atrial septal defect (ASD)?
An ASD is a defect in the atrial septum, leading to a left-to-right shunt. The most common type is ostium secundum.

54. What is patent ductus arteriosus (PDA) and what is it associated with?
PDA is the failure of the ductus arteriosus to close, causing a left-to-right shunt between the aorta and pulmonary artery. It is associated with congenital rubella.

55. What are the clinical features of PDA?
PDA is often asymptomatic at birth but is characterized by a continuous, “machine-like” murmur.

56. What is the treatment for PDA?
PDA is treated with indomethacin.

57. What are the four components of Tetralogy of Fallot, and what type of shunt does it involve?
Tetralogy of Fallot includes pulmonary stenosis, right ventricular hypertrophy, VSD, and an overriding aorta. It creates a right-to-left shunt, leading to cyanosis.

58. What is the characteristic X-ray finding of Tetralogy of Fallot (TOF)?
TOF is often associated with a “boot-shaped” heart on chest X-ray.

59. How can a patient with Tetralogy of Fallot alleviate symptoms?
Symptoms can be alleviated by squatting, which increases systemic vascular resistance.

60. What is transposition of the great vessels, and what is it associated with?
In this condition, the pulmonary artery arises from the left ventricle, and the aorta arises from the right ventricle. It leads to right ventricular hypertrophy and left ventricular atrophy. It is associated with maternal diabetes.

61. What is the treatment for transposition of the great vessels?
Treatment includes creating a shunt (such as using prostaglandin E to maintain PDA) and surgical repair.

62. Most congenital heart defects are due to abnormalities in which steps of fetal heart development?
They are due to abnormal development during the formation of the atria or ventricles, the division of the main outflow tract into the pulmonary trunk and aorta, and the development of the heart valves.

63. The fetal heart initially forms as what?
The fetal heart begins as a blood vessel that develops into an enlarged tube with three layers: endocardium, myocardium, and epicardium, along with cardiac jelly.

64. Cardiac jelly is a precursor to what structure?
Cardiac jelly is a precursor to endocardial cushion tissue.

65. How many chambers does the fetal heart initially have?
The fetal heart initially has one atrium and two ventricles.

66. What is the truncus arteriosus?
The truncus arteriosus is a single outflow tract that supplies the pulmonary trunk and aorta in fetal circulation.

67. What is the septum primum?
The septum primum is a structure formed by the superior and inferior endocardial cushions, which overlap to create the foramen ovale.

68. What is a shunt?
A shunt is an abnormal pathway that allows blood to flow through the heart or great vessels.

69. Which type of shunt is cyanotic?
A right-to-left shunt is cyanotic.

70. What are the two primary types of congenital heart disease?
The two primary types are shunts and obstructions.

71. What are the four main cyanotic congenital heart defects?
The four main cyanotic congenital heart defects are Tetralogy of Fallot, transposition of the great vessels, truncus arteriosus, and tricuspid atresia.

72. What is an abnormal communication between the atria?
An abnormal communication between the atria is known as an atrial septal defect (ASD).

73. What are the effects of an ASD on the heart?
ASD can lead to enlargement of the right atrium and right ventricle and may cause pulmonary hypertension if the defect is large.

74. What does the amount of shunting in a VSD depend on?
The amount of shunting in a VSD depends on the size of the defect and the degree of pulmonary vascular resistance.

75. Why is shunting limited in a small VSD?
Shunting is limited in a small VSD due to high resistance in the pulmonary vascular system.

76. What changes does a VSD cause in the heart?
A VSD leads to enlargement of the pulmonary artery, left atrium, and left ventricle due to increased blood flow.

77. How do the pulmonary vessels respond to VSD?
They undergo structural changes to limit blood flow to the lungs, a process that is irreversible. This raises pulmonary vascular resistance in an attempt to reduce the shunting.

78. What condition occurs when pulmonary pressure exceeds systemic pressure, causing the shunt to reverse?
Eisenmenger Syndrome.

79. What is the function of the ductus arteriosus in a fetal heart?
The ductus arteriosus allows blood to shunt from the pulmonary artery to the aorta, bypassing the lungs.

80. What should happen to the ductus arteriosus after birth?
As the lungs expand, the ductus arteriosus should constrict and close. If it remains open, it results in a patent ductus arteriosus (PDA).

81. In which direction does blood flow in a PDA?
Blood shunts left to right, from the aorta to the pulmonary artery.

82. What is coarctation of the aorta (COA)?
COA is a congenital heart defect characterized by a narrowing of the aortic lumen.

83. In a preductal COA, which chamber serves as the systemic pump?
The right ventricle functions as the systemic pump in preductal COA.

84. In COA, if aortic pressure is higher, what direction is blood shunted, and what are the effects?
Blood shunts left to right, increasing pulmonary blood volume and straining the left atrium and left ventricle.

85. In COA, if pulmonary artery pressure is higher, what direction is blood shunted, and what are the effects?
Blood shunts right to left, resulting in cyanosis and right ventricular hypertrophy.

86. What are the effects of pulmonary stenosis on the heart?
Pulmonary stenosis causes the right ventricle to struggle with pumping blood, leading to blood retention, increased afterload, and right ventricular hypertrophy.

87. What is pulmonary atresia?
Pulmonary atresia is a severe form of pulmonary stenosis, characterized by complete fusion of the pulmonary valve commissures.

88. What may occur with severe pulmonary stenosis and right-sided heart dilation and hypertrophy?
The foramen ovale may reopen to relieve pressure.

89. What are the effects of aortic stenosis on the heart?
Aortic stenosis increases the workload of the left ventricle, leading to hypertrophy, increased pressure in the left atrium, and fluid backup in the pulmonary circulation.

90. What are the four defects that compose Tetralogy of Fallot?
Tetralogy of Fallot includes a VSD high in the septum, an overriding aorta, pulmonary stenosis, and right ventricular hypertrophy.

91. How does a baby with transposition of the great arteries survive until surgery?
Survival requires another defect (such as PDA, ASD, or VSD) to allow some oxygenated blood to reach systemic circulation.

92. What are the consequences of truncus arteriosus?
In truncus arteriosus, the truncus arteriosus fails to divide, resulting in a single vessel supplying both systemic and pulmonary circulation, leading to mixed oxygenated and deoxygenated blood.

93. Where does most of the blood tend to flow in a truncus arteriosus defect?
Most blood flows to the pulmonary circulation, as it typically has lower pressure than systemic circulation.

94. What would be the effect of pulmonary stenosis in truncus arteriosus?
Pulmonary stenosis could raise pulmonary pressure above systemic levels, directing blood flow into the aorta instead.

95. What is tricuspid atresia?
Tricuspid atresia is a condition in which the tricuspid valve is imperforate, preventing blood flow between the right atrium and right ventricle.

96. For tricuspid atresia to be compatible with life, what other defects must be present?
Survival depends on additional defects such as ASD, a hypoplastic right ventricle, VSD, and PDA if the right ventricle is absent.

97. What is the result of a moderate to large ASD?
A moderate to large ASD can lead to pulmonary hypertension due to increased pulmonary blood flow.

98. In a fetus, which way does blood shunt through the PDA? How does this change in an adult?
In a fetus, blood shunts from the pulmonary artery to the aorta. In an adult, it typically shunts from the aorta to the pulmonary artery.

99. When does Tetralogy of Fallot develop?
Tetralogy of Fallot develops during embryonic development when the truncus arteriosus and ventricular septum are forming.

100. What other defects are often present with tricuspid atresia?
Associated defects include an ASD, a hypoplastic or absent right ventricle, an enlarged mitral valve and left ventricle, and pulmonary stenosis.

Final Thoughts

Congenital heart defects represent a spectrum of conditions with varying levels of impact on health and daily life. While the causes are not always known, early diagnosis and medical advancements have transformed the outlook for individuals with these conditions.

With proper treatment and ongoing care, many people born with congenital heart defects can lead fulfilling lives. By raising awareness and understanding the nature of these defects, we can continue to improve outcomes and support for those affected and their families.