CLINICAL UPDATE
Congenital “ holey ” hearts : Ventricular septal defect
By Dr Luigi D ’ Orsogna , Paediatric Cardiologist .
Western Cardiology . Tel 9346 9300
Ventricular septal defect ( VSD ) is the commonest congenital heart disease of childhood ( 55 % of cardiac defects in WA ). Single or multiple defects of the interventricular septum can be simply classified as membranous or muscular , and they can be isolated or associated with other defects like coarctation of the aorta or more complex malformations such as Tetralogy of Fallot . The pathophysiology and clinical manifestation of a VSD after birth is dependent on its size , the pulmonary vascular resistance ( PVR ) and the differential pressure between right and left ventricles .
Pathophysiology
Immediately after birth the PVR is high , hence there will be little flow across the VSD , which will be clinically “ silent ”. As the PVR diminishes over the ensuing days , flow increases across the defect . Small defects are not associated with symptoms but a typical pansystolic murmur at the lower left sternal border is audible ; smaller defects tend to produce louder murmurs as greater turbulence is created by the larger pressure difference between ventricles .
Conversely , excessive pulmonary blood flow from a large defect increases pulmonary artery pressure , which in turn raises the right ventricle pressure and diminishes the pressure difference across the VSD , thereby making the murmur less prominent .
� Fig 1 : 2 -dimensional echocardiogram ( apical 4 chamber view ) showing a large mid-muscular VSD ( arrow ).
� Fig2 : with AmplatzerTM VSD occlusive device in situ .
However , the newborn or young infant manifests symptoms and signs of excessive pulmonary blood flow : dyspnea and tachypnea that cause difficulty with feeding , tachycardia and hyperdynamic praecordial activity with or without a thrill , and an accentuated second heart sound with the pansystolic murmur . There may be an ejection systolic murmur at the left upper sternal border ( excessive flow across the pulmonary valve ) and a mid-diastolic murmur at the apex ( increased flow across the mitral valve ). If congestive cardiac failure develops , hepatomegaly is the best indicator at this age .
Investigation and treatment
Echocardiography is most accurate and informative . A small VSD requires no treatment as the defect may diminish or even close spontaneously ; most small muscular
VSDs close before school age and even moderate or large defects diminish enough in infancy so that no treatment will be needed .
However , if the infant with moderate or large VSD shows signs of not thriving or develops heart failure , then surgery will be required early , usually before six months of age . An asymptomatic moderate to large VSD requires elective closure later in infancy or early childhood to avoid the long-term complications of either pulmonary hypertension or volume overloaded left heart . Surgery is now relatively low risk with mortality < 1 %.
Transcatheter VSD device closure has limited application as it can only be used safely with muscular defects in older infants ; perimembranous defects are close to the cardiac valves and the conduction system , thereby risking their damage from an occlusive device .
Infective endocarditis prophylaxis is not required for VSD unless there has been previous endocarditis ( but it is required for six months after cardiac surgery / device closure ).
Declaration : Western Cardiology has contributed to the production costs of this clinical update . No author competing interests .
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