SUPERStudy: Ventricular Septal Defect
Introduction: Ventricular septal defect (VSD) is a hole in the wall that separates the right and left ventricles of the heart, resulting in shunt formation.
– They are the most prevalent congenital cardiac anomaly in children and the second most common in adults, surpassed only by bicuspid aortic valves.
Etiology: can occur with other congenital cardiac anomalies such as tetralogy of Fallot; associated with fetal alcohol syndrome, Down syndrome, maternal diabetes; as a complication of acute myocardial infarction.
Epidemiology: Isolated VSD constitutes 37% of all congenital heart diseases in children, with an incidence of approximately 0.3% among newborns. The occurrence diminishes significantly in adults due to the spontaneous closure observed in up to 90% of cases. There is no gender predilection.
Classification: –There are four types, classified by location: Outlet, membranous, inlet and the muscular.
Type A: Outlet tract VSD lies underneath the semilunar valves.
Type B: the membranous VSD has three variations
Type C: the inlet VSD is present below the tricuspid valve
Type D: the muscular VSD
-VSD sizes are defined by comparison to the aortic root size
-Muscular are the most common type
-Membranous VSD are the most common type requiring surgical intervention (80% of cases)
Pathophysiology: Defect in ventricular septum caused by failure of fusion of the interventricular septum with the aortic septum, leading to communication between right and left ventricles.
It allows oxygen-rich blood from the left ventricle flow into the right ventricle, which is pumped back to the lungs, even though this blood does not need oxygen. This puts more stress on the heart and lungs.
Initially, left-to-right shunt is present, due to lower pulmonary vasculature resistance as compared to systemic vascular resistance.Larger shunts may create both LV and RV volume and pressure overload. Later pulmonary hypertension may develop, leading to right heart failure, right-to-left shunt and cyanosis (Eisenmenger syndrome).
Clinical Manifestations
Small defects may be asymptomatic. Symptoms correlate with size and location.
Infants: failure to thrive, poor weight gain, sweating during feeding
Adults: Dyspnea, exercise intolerance, dizziness, feeling tired all the time, sweating
Complications: cyanosis with pulmonary hypertension, Eisenmenger syndrome, endocarditis, heart failure and arrhythmias
Heart murmur: A harsh holosystolic murmur at left lower sternal border in the third and fourth interspaces with a narrowly split second heart sound; RV heave
Diagnosis
Echocardiogram: confirms diagnosis
Chest X-ray: cardiomegaly, increased vascular markings; if pulmonary hypertension develops, an enlarged pulmonary artery with pruning of the distal pulmonary vascular bed
ECG: normal or right, left, or biventricular hypertrophy
RVH: Tall R waves in leads V1 and V2
LVH: Deep S waves in leads V2 and V3 and R waves in leads V5 and V6
Biventricular hypertrophy: Equiphasic QRS complexes in the mid precordial leads
Treatment
Small VSDs with small shunts (pulmonary to systemic flow ratio less than 1.5) in asymptomatic patients do not require surgery or other intervention.
Medium and large VSDs may need to be fixed with surgery or heart catheterization
| SUPERPoint: Ventricular septal defect (VSD) is the most common congenital heart defect, characterized by an abnormal opening in the interventricular septum, resulting in left-to-right shunting, increased pulmonary blood flow, and potential progression to pulmonary hypertension or Eisenmenger syndrome if untreated. |
| SUPERFormula: Patient reports dizziness, feeling tired, shortness of breath + a loud, harsh holosystolic murmurs in the left third and fourth interspaces along the sternum + CXR shows cardiomegaly, enlarged PA, increased vascular markings = Ventricular Septal Defect |