Patent Ductus Arteriosus (PDA)

• Increased pulmonary blood flow occurs when there is an abnormal connection between the left and right sides of the heart or between the great arteries, leading to recirculation of blood through the lungs.

Patent Ductus Arteriosus (PDA)

• PDA is a condition where the ductus arteriosus, a blood vessel connecting the pulmonary artery to the aorta in the fetus, fails to close after birth.
• This failure allows oxygenated blood from the aorta to flow into the pulmonary artery, increasing blood flow to the lungs.
• The increased pulmonary blood flow can lead to pulmonary hypertension, right ventricular hypertrophy, and eventually heart failure if left untreated.
• Clinical manifestations include a continuous "machine-like" heart murmur, bounding peripheral pulses, widened pulse pressure, and signs of heart failure such as tachypnea, dyspnea, and poor feeding.
• Diagnosis is typically made via echocardiography, which visualizes the ductus arteriosus and assesses the degree of left-to-right shunting.
• Management options include indomethacin or ibuprofen to promote ductal closure in premature infants, catheter-based closure devices, or surgical ligation for larger PDAs or when medical management fails.
• Prostaglandin inhibitors, like indomethacin, are effective in closing a PDA by inhibiting prostaglandin E1, which keeps the ductus open.
• Monitoring for complications such as necrotizing enterocolitis (NEC) and renal dysfunction is crucial during indomethacin or ibuprofen treatment.
• In some cases, maintaining a patent ductus arteriosus is desirable, such as in infants with certain cyanotic heart defects where PDA allows for systemic blood flow; in these cases, prostaglandin E1 is administered to keep the ductus open.
• The long-term prognosis after PDA closure is generally excellent, with normal growth and development expected.

Atrial Septal Defect (ASD)

• ASD is a congenital heart defect characterized by an opening in the atrial septum, allowing blood to flow between the left and right atria.
• This results in oxygenated blood from the left atrium shunting to the right atrium, increasing pulmonary blood flow.
• Most individuals with ASD are asymptomatic in childhood, with symptoms potentially developing in adulthood.
• The most common symptom in adults is exertional dyspnea, but other symptoms may include fatigue, palpitations, and right heart failure.
• A fixed, widely split second heart sound is a classic auscultatory finding in ASD due to the increased volume in the right ventricle delaying closure of the pulmonic valve.
• Echocardiography is the primary diagnostic tool, allowing visualization of the defect and assessment of the shunt volume.
• Small ASDs may close spontaneously, while larger defects typically require intervention.
• Transcatheter closure with a septal occluder device is the preferred method for most secundum ASDs (the most common type), while surgical closure may be necessary for larger or more complex defects.
• Complications of untreated ASD can include pulmonary hypertension, atrial arrhythmias, and paradoxical embolization.
• Post-closure, individuals typically have normal cardiac function and life expectancy.
• Regular follow-up is important to monitor for any late complications, such as arrhythmias.

Ventricular Septal Defect (VSD)

• VSD involves an abnormal opening in the ventricular septum, allowing blood to flow between the left and right ventricles.
• This leads to oxygenated blood from the left ventricle shunting to the right ventricle, increasing pulmonary blood flow.
• The clinical presentation varies depending on the size and location of the VSD.
• Small VSDs may be asymptomatic or cause only a murmur, while large VSDs can lead to heart failure in infancy.
• A holosystolic murmur is typically heard at the left sternal border.
• In large VSDs, infants may present with poor weight gain, diaphoresis with feeding, and respiratory distress.
• Echocardiography is used to diagnose VSD, determine its size and location, and assess the degree of shunting and pulmonary artery pressure.
• Some small VSDs may close spontaneously in early childhood.
• Medical management for symptomatic VSD includes diuretics to reduce fluid overload and digoxin to improve contractility.
• Surgical repair, involving patching the defect, is indicated for large VSDs causing significant symptoms or pulmonary hypertension.
• Transcatheter closure is an option for certain types of VSDs, but less commonly used than surgical repair.
• Complications of untreated VSD include Eisenmenger syndrome (development of irreversible pulmonary hypertension due to chronic increased pulmonary blood flow), infective endocarditis, and aortic valve regurgitation.
• After surgical or transcatheter closure, most individuals have excellent long-term outcomes.
• Regular follow-up is necessary to monitor for complications such as arrhythmias or residual VSD.