Share This Link

Ventricular septal defect is a left-to-right shunt that increases pulmonary blood flow rather than obstructing systemic output. While large defects can cause exercise intolerance due to heart failure, they do not typically present with angina or dizziness. The primary symptoms involve tachypnea and poor weight gain in younger children. It is not an obstructive lesion.

Mitral valve prolapse is often asymptomatic or presents with vague palpitations and atypical chest pain that is not usually exertional. It involves the displacement of the mitral valve leaflets into the left atrium during systole. While common in adolescents, it does not typically cause the severe obstructive symptoms of syncope and exertional angina. It rarely restricts activity significantly.

Tricuspid atresia is a severe cyanotic heart defect where the tricuspid valve fails to develop. This results in decreased pulmonary blood flow and profound hypoxemia from birth. Children with this condition usually have a history of multiple palliative surgeries and baseline cyanosis. It does not manifest as new-onset exertional dizziness in a previously healthy school-aged child.

Indomethacin is a nonsteroidal anti-inflammatory drug that acts as a prostaglandin inhibitor. It is used clinically to facilitate the closure of a patent ductus arteriosus in premature infants. Administering this to a neonate with critical aortic stenosis would be fatal as it would eliminate the only route for systemic blood flow. It is strictly contraindicated in ductal-dependent obstructive lesions.

Acetaminophen is an analgesic and antipyretic medication used to manage pain and fever. While safe for general use in neonates, it has no hemodynamic properties and does not affect the patency of fetal heart structures. It would be ineffective in addressing the primary pathophysiological crisis of systemic hypoperfusion. It lacks the pharmacological action required to manage an aortic obstruction.

Albuterol is a beta-2 agonist used to treat bronchospasm and improve airway resistance in respiratory conditions. It acts on the smooth muscle of the bronchioles rather than the vascular smooth muscle of the aorta or ductus arteriosus. It plays no role in the management of congenital heart defects or the maintenance of systemic circulation. It would not resolve the underlying cardiac output deficiency.

Pulmonary edema is a clinical sign of congestive heart failure that occurs when the left ventricle fails. While it can occur in advanced stages of untreated stenosis, it is a secondary complication of pump failure. It is not the most immediate structural risk compared to the compensatory thickening of the heart wall.

Right-sided heart failure typically occurs as a sequela to long-standing left-sided failure or primary pulmonary disease. In isolated aortic stenosis, the primary pathological stress is localized to the left side of the heart. Right-sided involvement only happens after pulmonary hypertension develops due to chronic left-sided congestion.

Increased pulmonary blood flow is characteristic of acyanotic left-to-right shunts, such as a ventricular septal defect. Aortic stenosis is an obstructive lesion and does not involve an abnormal opening that redirects blood to the lungs. Instead, it creates a bottleneck for blood trying to exit the heart into the systemic circulation.

Blood does not flow directly from the lungs into the aorta. In a normal heart, and in aortic stenosis, blood travels from the lungs to the left atrium, then the left ventricle, and then into the aorta. This choice describes an incorrect anatomical pathway.

Blood mixing between the atria is the definition of an atrial septal defect (ASD). Aortic stenosis is a valvular problem on the left side of the heart; it does not typically involve a hole or "mixing" between the upper chambers of the heart.

Pulmonary circulation becoming overloaded is characteristic of left-to-right shunts, such as a ventricular septal defect (VSD) or patent ductus arteriosus (PDA). While severe, long-term aortic stenosis can eventually cause backup into the lungs, its primary pathophysiology is an outflow obstruction, not a volume overload of the pulmonary circuit.