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(HR. Muslim, Ahmad dan Hakim).

Jumat, 01 Januari 2010

Ventricular Septal Defect


A ventricular septal defect (VSD) is a congenital abnormal opening in the ventricular septum that allows communication of blood between the left and right ventricles. VSDs are caused by embryologic malformations of the ventricular septum. They can occur as an isolated lesion or in combination with other congenital cardiac anomalies. The defect can range from a lesion that might require surgery to a miniscule hole in the muscular septum. Blood flow across the defect is typically left to right and depends on the size of the defect and the pulmonary vascular resistance (PVR).
History of the Procedure

In 1950, Bailey first attempted pulmonary artery banding for the treatment of VSDs. Three years later, he attempted direct suture of a VSD using hypothermia and vena caval occlusion. In 1956, Kirklin reported the first cases of direct-vision intracardiac repair of VSDs using the mechanical pump oxygenator. In 1957, Lillehei demonstrated the feasibility of the transatrial approach to VSD repair using cardiopulmonary bypass.

VSDs rank first in frequency on all lists of cardiac defects. They account for 25-40% of all cardiac malformations at birth. US and international frequencies are identical—approximately 1-2 cases per 1000 live births. Studies have shown that the prevalence of VSDs has increased in the United States during the past 30 years. A twofold increase in the prevalence of VSD was reported by the Centers for Disease Control and Prevention from 1968-1980. The Baltimore-Washington Infant Study (BWIS) reported a twofold increase in the prevalence of VSD from 1981-1989. The BWIS study reported that the increase is primarily attributed to more sensitive detection through echocardiography.

VSDs result from a deficiency of growth or a failure of alignment or fusion of component parts of the ventricular septum. Incomplete closure of the interventricular foramen and failure of the membranous part of the interventricular septum to develop result from failure of tissue to grow from the right side of the fused endocardial cushions and to fuse with the aorticopulmonary septum and muscular part of the interventricular septum.

The increase of alcohol and illicit drug use has been identified as possible risk factors for VSD. The National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention produced data that show maternal marijuana use during the preconception period is associated with an increased risk of simple VSD. The study goes on to show an increase in use correlated with an increase in VSD prevalence.

A twofold increase in the risk of VSD associated with maternal cocaine use during pregnancy was found in a study at Boston City Hospital in 1991. The BWIS further reported correlations between membranous isolated VSD and paternal cocaine use. Abnormal blood flow to the heart due to the vasoconstricting effects of cocaine is a postulated reason for these increases.

Finally, alcohol consumption has also been associated with increased VSD. The BWIS found that maternal alcohol consumption was associated with small muscular VSD. No correlation was found with membranous VSDs. A study from Finland further found that alcohol consumption was associated with a 50% increase in VSDs.

Correlations are not detected between the muscular VSDs and maternal use of NSAIDs or acetaminophen. Such correlations were also not detected between maternal fever and VSDs.

The VSD permits a left-to-right shunt to occur at the ventricular level. A left-to-right shunt at the ventricular level has 3 adverse hemodynamic consequences: (1) left ventricular (LV) volume overload, (2) increased pulmonary blood flow, and (3) compromise of systemic cardiac output.

The functional disturbance caused by a VSD depends on the magnitude of the shunt, which is a function of the size of the VSD and the status of the pulmonary vascular bed rather than the location of the VSD. A small VSD with high resistance to flow permits only a small left-to-right shunt. A large interventricular communication allows a large left-to-right shunt only if no pulmonic stenosis or high PVR exists because these factors also determine shunt flow. Quantifying the shunt by the ratio of pulmonary-to-systemic circulation (QP/QS) is useful.

The severity of pulmonary vascular disease correlates to the size of the shunt. In time, as PVR increases, irreversible histologic changes may occur within the pulmonary vascular bed. Untreated, a reversal of the flow occurs, leading to a right-to-left shunt with the development of increasing cyanosis (Eisenmenger complex).

The natural history of VSDs encompasses a wide spectrum, ranging from spontaneous closure to congestive cardiac failure and death in early infancy. The spectrum includes possible development of pulmonary vascular obstruction, right ventricular (RV) outflow tract obstruction, aortic regurgitation, and infective endocarditis.

The clinical picture and functional impairment of VSDs primarily depend on the size of the defect, the status of the pulmonary vasculature, and the degree of shunting, and less on the location of the VSD. Note the following features:
A small VSD usually causes no symptoms.
Respiratory distress and mild tachypnea result from abnormal pulmonary compliance due to mild left-to-right shunting.
Because of compromised systemic output and vasoconstriction, infants with moderately sized VSDs may be pale and are often diaphoretic.
Patients with moderately sized VSDs and decreased pulmonary compliance frequently have a history of 1 or more episodes of pneumonia and/or upper respiratory tract infections.
Infants with a large left-to-right shunt often have congestive heart failure and fail to gain weight.
Patients with VSDs complicated by pulmonary hypertension and reversed shunts (ie, Eisenmenger complex) may present with exertional dyspnea, chest pain, syncope, hemoptysis, cyanosis, clubbing, and polycythemia.
Bacterial endocarditis can develop regardless of the size of the VSD and is related to turbulent blood flow through the defect.
The most common physical finding is a harsh grade IV-VI holosystolic murmur. The murmur is best heard along the left sternal border, is usually louder at the third and fourth intercostal spaces, and is widely transmitted over the precordium. The murmur of VSD does not radiate to the left axilla, as with mitral regurgitation, and does not increase in intensity with inspiration, as with tricuspid regurgitation.
Generally, the smaller the defect, the more turbulent the blood flow through it and the louder the murmur. A grade V-VI murmur may be associated with a very high-velocity flow through only a small, hemodynamically insignificant VSD.
A systolic thrill can commonly be palpated in the region of the murmur along the lower left sternal border. A systolic thrill is less common with large VSDs than with moderate or small defects.
Large defects, with appreciable left-to-right shunts, have wide splitting of the S2, which varies with respiration, and the pulmonic component is accentuated.
When the left-to-right shunt is large, a diastolic, low-pitched flow rumble, suggesting increased flow through the mitral valve, is present. This rumble, which is audible at the lower left sternal border, is often associated with LV S3 gallop.
If pulmonary hypertension develops, the holosystolic murmur diminishes and the thrill disappears. In these patients, the pulmonic component of S2 becomes loud, and an RV lift (indicative of RV hypertrophy) may develop. Cyanosis may become evident, and polycythemia follows. A pulmonary ejection sound may also be noted. The murmur of pulmonary insufficiency can develop (ie, Graham Steell murmur).
Supracristal VSDs in the outlet septum may produce murmurs and thrills more prominent in the first or second left intercostal space with radiation upward.
Patients with a supracristal VSD may develop a diastolic blowing murmur of aortic regurgitation. The holosystolic murmur followed immediately by a blowing diastolic murmur may simulate a continuous murmur.
Patients with VSD are especially at risk for endocarditis, pulmonary infection, ventricular arrhythmias, heart failure, and pulmonary hypertension.
Of patients with congenital VSD, 20% have additional cardiac abnormalities. Most abnormalities were detected at the initial assessment stage; however, aortic prolapse and pulmonary stenosis may also develop subsequently.
Aortic regurgitation may result from the high velocity flow beneath a poorly supported right aortic cusp.

The indications for surgical intervention and its timing may be simple or complex. While many investigators have tried to establish an algorithm for management, the decision to intervene is often a combination of the judgment of pediatric cardiologists and surgeons. The approach must carefully consider the patient's age, symptoms, physiology, and anatomy. Many areas are open to interpretation.
Symptomatic infants with large shunts who cannot be managed medically should undergo closure of the defect.
Surgical repair in patients younger than 6 months is undertaken for control of intractable congestive heart failure, recurrent lower respiratory tract infections, or failure to thrive despite medical treatment.
In children younger than 2 years, prompt surgical repair is indicated if pulmonary hypertension begins to develop before an inoperable predominant right-to-left shunt ensues.
Criteria for surgery in children older than 2 years include presence of symptoms, a QP/QS greater than 2:1, cardiomegaly, or elevated pulmonary artery pressure (PAP).
In adults, surgery is usually recommended if the QP/QS is more than 1.5:1. Once the PVR exceeds 60-70% of systemic vascular resistance and the left-to-right shunt diminishes, closure of the ventricular septal defect (VSD) may no longer be indicated.
Surgery is not indicated in asymptomatic patients with normal findings on chest radiographs and ECGs and a QP/QS of less than 1.5:1.
Patients with subarterial VSD and aortic cusp prolapse, supracristal VSD with aortic regurgitation, or perimembranous VSD with aortic regurgitation are ordinarily referred for surgery to prevent progression of aortic regurgitation.
Even small VSDs should be closed after a single episode of infective endocarditis if the defect remains open once the infection has been cured.
Relevant Anatomy

Ventricular septal defects (VSDs) are classified by the position they occupy in the ventricular septum. The septum is divided into 4 components: the membranous septum, the inlet, the trabecular, and the outlet parts of the muscular septum. (The outlet septum is also called the conal or infundibular septum.) Thus, 4 anatomic types of VSDs exist.
Type I defects are also known as subarterial, outlet, or conal defects. These defects comprise 5% of all VSDs and are located in the outlet portions of the left and right ventricles. The superior edge of the VSD is the conjoined annulus of the aortic and pulmonary valves. Because the aortic and pulmonary valves are in fibrous continuity, this type of defect may also be referred to as doubly committed subarterial. (They are also called juxta-arterial, supracristal, subpulmonary, infundibular, or conoseptal defects.) This VSD is associated with prolapse of the unsupported aortic valve cusps and progressive aortic regurgitation.
Type II defects are also called infracristal, subaortic, perimembranous, or paramembranous defects. These defects are the most common type of VSD, comprising 75% of all VSDs. They occur around the membranous septum and the fibrous trigone of the heart and are associated with a muscular defect at a portion of their perimeter. The defect is near the aortic valve, and the annulus of the tricuspid valve contributes to the rim of the defect. Perimembranous defects are divided into 3 major subtypes according to the adjacent portion of the muscular septum: perimembranous inlet, perimembranous trabecular, and perimembranous outlet.
Type III defects (10% of all VSDs), also called atrioventricular (AV) canal, AV septal, or inlet septal defects, are located in the posterior region of the septum beneath the septal leaflet of the tricuspid valve.
Type IV defects (10% of all VSDs), also called muscular defects, have entirely muscular rims. They may be single but are commonly multiple. Muscular defects may be divided into several categories: inlet, trabecular, central, apical, marginal, and outlet (infundibular). Most commonly, multiple defects occur in the apical trabecular septum. In its most severe form, multiple defects of the ventricular septum are sometimes descriptively referred to as Swiss cheese septum.

A pulmonary-to-systemic vascular resistance ratio greater than 0.9:1 or pulmonary arteriolar resistance greater than 12 Wood units is regarded as an absolute contraindication to surgery.
Pulmonary hypertension is not a contraindication to surgery provided the pulmonary-to-systemic vascular resistance is less than 0.75:1. Furthermore, PVR may be described as reactive when it is lowered by higher inspired oxygen content or vasodilators such as nitric oxide. Nonresponders are described as fixed. Patients whose PVR is reactive may benefit more from repair than those whose PVR is fixed.
A PVR of more than 8 Wood units obtained during cardiac catheterization with pulmonary vasodilatation is a contraindication to surgery.


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