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Ventricular Septal Defect

A ventricular septal defect (VSD) is an abnormal opening between the left and right ventricles that allows blood to pass between the ventricles. It is the most common type of congenital heart defect. Blood flows from the high pressure left ventricle through the VSD into the lower pressure right ventricle, resulting in excessive blood flow to the lungs. Small VSDs often close on their own and cause no symptoms, while larger VSDs can cause symptoms like difficulty breathing, failure to thrive, and heart failure if not treated. Treatment depends on the size of the VSD and symptoms, ranging from monitoring to device closure or open heart surgery to close the defect.

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246 views

Ventricular Septal Defect

A ventricular septal defect (VSD) is an abnormal opening between the left and right ventricles that allows blood to pass between the ventricles. It is the most common type of congenital heart defect. Blood flows from the high pressure left ventricle through the VSD into the lower pressure right ventricle, resulting in excessive blood flow to the lungs. Small VSDs often close on their own and cause no symptoms, while larger VSDs can cause symptoms like difficulty breathing, failure to thrive, and heart failure if not treated. Treatment depends on the size of the VSD and symptoms, ranging from monitoring to device closure or open heart surgery to close the defect.

Uploaded by

AisyahKautsarIlmi
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOC, PDF, TXT or read online on Scribd
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VENTRICULAR SEPTAL DEFECT

A VSD is an abnormal communication between the right and left ventricles. It is the
most common type of congenital heart defect, accounting for approximately 2! of
all "#Ds. VSDs vary in the si$e %small and restrictive to large and nonrestrictive
defect&, number %single versus multiple&, and type %perimembranous or muscular&.
Pathophysiology and Etiology
'lood flows from the high(pressure left ventricle across the VSD into the low(
pressure right ventricle and into the )A, resulting in pulmonary
overcirculation.
A left(to(right shunt because of a VSD results in increased right ventricular
pressure and increased )A pressure.
*he increased pulmonary venous return to the left side of the heart results in
left atrial dilation.
+ong(standing pulmonary overcirculation causes a change in the pulmonary
arterial bed, leading to increased pulmonary vascular resistance. #igh
pulmonary vascular resistance %)V,& can reverse the blood flow pattern that
leads to a right(to(left shunt across the VSD %-isenmenger.s syndrome&,
resulting in cyanosis. /nce this develops, the child is no longer a candidate for
surgical repair.
Clinical Manifestations
Small VSDs012usually asymptomatic3 high spontaneous closure rate during
the first year of life.
+arge VSDs.
o "#45 tachypnea, tachycardia, excessive sweating associated with
feeding, hepatomegaly.
o 4re6uent 7,Is.
o )oor weight gain, failure to thrive.
o 4eeding difficulties.
o Decreased exercise tolerance.
Diagnostic Eal!ation
Auscultation5 harsh systolic regurgitant murmur heard best at the lower left
sternal border %++S'&3 systolic thrill felt at ++S', narrowly split S
2
.
"hest 8(ray5 varies3 normal or cardiomegaly and increased pulmonary
vascular mar9ings. )ulmonary vascular mar9ings are directly proportionate to
the amount of left(to(right shunting.
-":5 varies3 normal to biventricular hypertrophy.
*wo(dimensional echocardiogram with Doppler study and color flow mapping
to identify the si$e, number, and sites of the defects, estimate pulmonary artery
pressure, and identify associated lesions.
"ardiac catheteri$ation usually not needed for initial diagnosis3 may be needed
to calculate the si$e of the shunt or to assess )V,. ;ay be performed if defect
can be closed using a ventricular occlusion device %device can be used only in
muscular defects&.
Manage"ent
Small VSD
;edical management5
o 7sually no anticongestive therapy is needed.
o Infective endocarditis prophylaxis for < months after surgical
implantation of a ventricular occlusion device.
"ardiac catheteri$ation for placement of a ventricular occlusion device for
muscular defects %for =p5=s > 25?&.
Surgical intervention is usually not necessary.
;oderate to +arge VSD
;edical ;anagement5
o "#4 management5 digoxin and diuretics %furosemide, spironolactone&
and afterload reduction.
o Avoid oxygen3 oxygen is a potent pulmonary vasodilator and will
increase blood flow into the )A.
o Increase caloric inta9e5 fortify formula or breast mil9 to ma9e 2@ to AB
calCo$ formula3 supplemental nasogastric feeds as needed.
o Infective endocarditis prophylaxis for < months after
surgeryCventricular device occluder.
"ardiac catheteri$ation for placement of a ventricular occlusion device for
muscular defects %for =p5=s > 25?&.
,efer for surgical intervention.
o 7sually repaired before age ?.
o /ne(stage approach5 preferred surgical plan3 patch closure of VSD.
o *wo(stage approach5 first surgery is to band the )A to restrict
pulmonary blood flow3 second surgery is to patch close the VSD and
remove the )A band.
+ong(*erm 4ollow(7p
;onitor ventricular function.
;onitor for subaortic membrane and double(chamber ,V.
Co"plications
"#4.
4re6uent 7,Is.
4ailure to thrive3 poor weight gain.
Infective endocarditis.
-isenmenger.s syndrome.
)ulmonary hypertension.
Aortic insufficiency.

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