Ventricular septal defect causes left ventricular volume overload
the verdict
INSUFFICIENT LEANING
refutedsupported
the weight of evidence
2 sources for · 0 against
The retrieved literature mentions ventricular septal defects and related shunting patterns, but provides only partial or tangential coverage regarding left ventricular volume overload.
In patients with concomitant right ventricular volume overload, flow across the ventricular defect was from the right to the left ventricle throughout diastole in 30 (86%) of 35 studies. In each of four patients with d-transposition of the great vessels and each of two patients with 1-transposition of the great vessels, blood flow was from the morphologic left ventricle to the morphologic right ventricle during isovolumetric contraction and from the morphologic right ventricle to the morphologic left ventricle during isovolumetric relaxation. These results demonstrate 1) the complex nature of intracardiac shunting in children with ventricular septal defect as previously shown by angiography; 2) an intrinsic functional difference in the contractile and relaxation properties of the morphologic left and right ventricles; and 3) differences in diastolic blood flow patterns between children with an isolated defect and those with a ventricular septal defect and right ventricular volume overload (p = 0.0001). Published in Journal of the American College of Cardiology (1990)
A ventricular septal defect (VSD) is a hole in the ventricular septum, the wall dividing the left and right ventricles of the heart. It is a common congenital
A ventricular septal defect (VSD) is a hole in the ventricular septum, the wall dividing the left and right ventricles of the heart. It is a common congenital heart defect, although restrictive muscular VSDs are not true pathological defects; they are typically just a delayed closure of the ventricular septum. They have an extremely high prevalence in newborns. The extent of the opening may vary f
Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.
The restrictive ventricular septal defects (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.
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