Why pansystolic murmur in vsd

This can be a congenital anomaly or acquired as a complication of a myocardial infarction. Ventricular septal defects are classified as membranous, perimembranous, supracristal infundibular or subpulmonic or muscular. Enlarge Membranous VSDs are the most common type and originate inferior to the crista supraventricularis, yet still towards the left ventricular outflow tract.

Perimembranous VSDs are also inferior to the crista supraventricularis, however extend into the muscular septum. Supracristal VSDs occur just beneath the aortic valve at the left ventricular outflow tract. A Venturi effect can occur from the left to right shunt causing the aortic valve leaflet to prolapse into the VSD resulting in significant aortic valve regurgitation. Muscular VSDs occur in the mid to apical interventricular septum and do not involve cardiac valves. The magnitude of the shunt depends on defect size and downstream resistance ie, pulmonary outflow tract obstruction and pulmonary vascular resistance.

In nonrestrictive ventricular septal defects, blood flows easily across larger defects; pressure equalizes between the right and left ventricles and there is a large left-to-right shunt. Assuming there is no pulmonic stenosis, over time, a large shunt causes pulmonary artery hypertension Pulmonary Hypertension Pulmonary hypertension is increased pressure in the pulmonary circulation.

It has many secondary causes; some cases are idiopathic. In pulmonary hypertension, pulmonary vessels become constricted Ultimately, the increased pulmonary vascular resistance causes shunt direction to reverse from the right to the left ventricle , leading to Eisenmenger syndrome Eisenmenger Syndrome Eisenmenger syndrome is a complication of uncorrected large intracardiac or aortic to pulmonary artery left-to-right shunts.

Increased pulmonary resistance may develop over time, eventually Restrictive ventricular septal defects, which are smaller defects, limit the flow of blood and the transmission of high pressure to the right heart.

Small VSDs result in a relatively small left-to-right shunt, and pulmonary artery pressure is normal or minimally elevated. Heart failure, pulmonary hypertension, and Eisenmenger syndrome do not develop. Symptoms depend on defect size and magnitude of the left-to-right shunt. Children with a small ventricular septal defect are typically asymptomatic and grow and develop normally. Frequent lower respiratory tract infections may occur.

Eventually, untreated patients may develop symptoms of Eisenmenger syndrome. Auscultatory findings vary with the size of the defect. Hearing-impaired health care practitioners can use amplified stethoscopes The precordium is not hyperactive, and the 2nd heart sound S2 is normally split and has normal intensity. Moderate to large VSDs produce a holosystolic murmur that is present by age 2 to 3 weeks; S2 is usually narrowly split with an accentuated pulmonary component.

An apical diastolic rumble due to increased flow through the mitral valve and findings of heart failure eg, tachypnea, dyspnea with feeding, failure to thrive, gallop, crackles, hepatomegaly may be present. In moderate, high-flow VSDs, the murmur is often very loud and accompanied by a thrill grade 4 or 5 murmur.

With large defects allowing equalization of left ventricular and right ventricular pressures, the systolic murmur is often attenuated. Comments Icon Comments 0. View full article. Sign in Don't already have an account? Individual Login. Institutional Login. Sign in via OpenAthens. Pay-Per-View Access. Buy This Article. View Your Tokens. View Metrics. Even in patients who respond to medical management, the presence of Down Syndrome necessitates early surgery to prevent the development of pulmonary hypertension.

If surgery cannot be performed in a symptomatic patient, pulmonary arterial banding may help limit the pulmonary blood flow until surgical repair is possible. Some Rights Reserved. Date last modified: July 7, Ashraf Aly and Soham Dusgupta Dept.

SoftChalk About this book Chapter Index. Figure showing a ventricular septal defect Pathophysiology With a small sized VSD , "restrictive VSD," the direction and magnitude of the shunt depends on the size of the VSD and the pressure gradient between the left and right ventricles. The intensity of the murmur is inversely proportional to the magnitude of the shunt; the smaller the shunt, the louder the murmur and vice versa. A decrescendo early systolic murmur may indicate a small and closing VSD.

There is diminished flow in the latter part of systole and no murmur is heard. An apical mid-diastolic murmur rumble may be heard due to increased flow across the mitral valve relative mitral stenosis. This indicates that the VSD is large enough to cause excessive pulmonary blood flow and this clinically indicates congestive heart failure CHF. This CHF is not due to pump dysfunction as in adults but due to the increased pulmonary blood flow.

An early diastolic murmur heard at the upper left sternal border in a sitting position could be heard in a small membranous or a supra-cristal VSD. This indicates aortic insufficiency due to prolapse of one of the aortic valve cusps into the VSD secondary to the suction created by the high velocity jet Venturi effect. A loud P2 with narrow splitting of S2 indicates increased pulmonary vascular pressure and resistance which would cause early closure of the pulmonary valve.

An early diastolic murmur due to pulmonary insufficiency may be heard if pulmonary hypertension develops. Pulmonary hypertension diminishes the pulmonary blood flow and makes CHF unlikely honeymoon before the development of Eisenmenger syndrome.

Cardiomegaly and hepatomegaly may be present if CHF is present. Chest radiographs may show cardiomegaly and increased pulmonary vascularity. The right atrium is usually unaffected. Echocardiogram shows the location, type and size of the VSD.

It can also estimate the pressure gradient across the VSD. The hemodynamic effects of VSD on different chambers can be elucidated. It is also important to look for aortic insufficiency especially in membranous and supra-cristal VSD which may indicate an early damage to the aortic valve.

Management Asymptomatic children with a small or medium sized VSD need only supportive care, with the expectation that the VSD will close in the first few years of life.

Patent Ductus Arteriosus Anatomy Anatomy The ductus arteriosus, formed from the embryonic 6th aortic arch, connects the aorta to the pulmonary artery.

Figure showing a Patent Ductus Arteriosus Pathophysiology Failure of closure of the ductus arteriosus leads to hemodynamic changes similar to those seen in VSD. Clinical presentations PDA is more common in females, premature infants, patients with Down Syndrome and congenital rubella syndrome. Making the diagnosis In older children, PDA classically produces a continuous or "machinery" murmur due to flow across the shunt throughout the cardiac cycle.

In newborn infants, especially those born prematurely, the murmur may be heard only during systole because the higher pulmonary arterial pressure diminishes flow during diastole. An apical mid-diastolic murmur may be heard because of increased flow through the mitral valve relative mitral stenosis. Wide pulse pressure indicates a large left-to-right shunt due to a sudden drop in diastolic pressure.

In a large PDA, the EKG will demonstrate right ventricular hypertrophy, left ventricular and left atrial enlargement due to volume overload. Chest radiographs may show increased pulmonary vascularity and cardiomegaly due to left atrial and left ventricular enlargement. The heart size might be normal if the shunt is small. Natural history and management Small and moderate sized PDA often close spontaneously especially in full term infants.