membranosus vsd

8/10/2019 Membranosus VSD

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Background

Perimembranous ventricular septal defects (VSDs) are located in the left ventricle outflow tract beneath the aortic valve. They are the most common VSD subtype in the United States,occurring in 75-80% of cases. Defects may extend into adjacent portions of the ventricularseptum. When tissue forms on the right ventricular septal surface (often thought to beatrioventricular valvular in origin), it is termed an aneurysm of the membranous septum. Suchtissue serves as a mechanism of spontaneous closure. The defect may be partially or completelyoccluded by the septal leaflet of the tricuspid valve. (See Epidemiology, Prognosis, andTreatment.)

Normal closure of the ventricular septum occurs through multiple concurrent embryologicmechanisms that help to close the septums membranous portion: (1) downward growth of theconotruncal ridges forming the outlet septum, (2) growth of the endocardial cushions forming theinlet septum, and (3) growth of the muscular septum forming the apical and midmuscular

portions of the septum.

Ventricular septal defects (VSDs) occur when any portion of the ventricular septum does notcorrectly form or if any of components do not appropriately grow together. The ventricularseptum is complete by 6 weeks' gestation. VSDs are typically classified according to the locationof the defect in 1 of the 4 ventricular components: the inlet septum, trabecular septum,outlet/infundibular septum, or membranous septum. This article specifically addresses defects inthe trabecular muscular septum . (See Etiology.)

Small VSDs (defined as VSD dimension less than half the size of the aortic annulus diameter)are usually isolated defects with otherwise normal cardiac anatomy and function. Large VSDs(defined as defect size equal to the diameter of the aortic annulus) typically have left atrial andleft ventricular dilation with normal left ventricular systolic function. (See Workup.)

Perimembranous VSD is caused by failure of the endocardial cushions, the conotruncal ridges,and the muscular septum to fuse at a single point in space.

Hemodynamic effects of VSD

Independent of the type of ventricular septal defect (VSD), the hemodynamic significance of theVSD is determined by 2 factors: the size of the defect and the resistance to flow out of the rightventricle, including the pulmonary vascular resistance (PVR) and anatomic right ventricularoutflow obstruction.

In small to moderate VSDs, left-to-right shunting is primarily limited by the size of the defect.Conversely, in large VSDs without right ventricular outflow obstruction, the left-to-rightshunting is determined by the relative degree of PVR and systemic vascular resistance.

Because PVR is high at birth and does not reach its nadir until age 6-8 weeks, the developmentof significant left-to-right shunting and pulmonary overcirculation, often termed congestive heartfailure (CHF), can be delayed until the second or third month of life. Additional cardiac lesions
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that increase left-to-right shunting (eg, atrial septal defect, patent ductus arteriosus) may predispose patients to earlier development of CHF. Noncardiac abnormalities, including prematurity, infection, anemia, and other congenital anomalies, also may predispose infants tosignificant symptoms of heart failure.

Additional congenital heart lesions (eg, muscular right ventricular outflow tract obstruction, pulmonary valve stenosis, pulmonary venous obstruction, persistent elevation of PVR, mitralstenosis) can restrict shunting, possibly leading to right-to-left trans-VSD flow, depending on theultimate resistance balance between the systemic and the total right-sided resistances.

Complications

Complications may include the following (see Prognosis):

CHF Bacterial endocarditis

Eisenmenger syndrome Aortic insufficiency Subaortic stenosis Double-chambered right ventricle

Patient education

Advise the patient and/or his or her parents regarding the risks of bacterial endocarditisindications and the importance of oral hygiene. Educate them concerning signs and symptoms ofCHF.

For patient education information, see the Heart Health Center , as well as Congestive HeartFailure and Ventricular Septal Defect .

Etiology

Perimembranous VSDs have a multifactorial etiology and are predominantly the result ofspontaneous abnormalities in development. The precise etiology of muscular septal defectformation is unknown. However, the proposed mechanisms are many. Muscular defects mayoccur because of a lack of merging in the walls of the trabecular septum or because of excessiveresorption of muscular tissue during ventricular growth and remodeling.

No significant correlation between the cause of VSDs and the age of the mother or the birthorder of the child is observed.

VSDs are the most common congenital heart lesion associated with chromosomal anomalies andsyndromes. VSDs are especially common in patients with trisomy 13, trisomy 18, and trisomy21. However, nearly 95% of VSDs are not associated with chromosomal abnormalities.

Noncardiac conditions associated with VSD include prematurity.
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Regular maternal cannabis use slightly increases the incidence of VSD .[1] The use of selectiveserotonin reuptake inhibitors (SSRIs) during early pregnancy also slightly increases theincidence of VSD .[2]

Epidemiology

Occurrence in the United States

Without regard to type, VSD is the most common congenital heart defect in the first 3 decades oflife, with an incidence between 1.5-4.2 cases for every 1000 live-term infants. VSD is morecommon in premature infants with an incidence of 4.5-7 cases for every 1000 liveborn infants.

Clinically significant VSD that requires medical or surgical management accounts for only 15%of such defects (0.35-0.50 cases for every 1000 live births). When viewing congenital heartdisease in total, solitary VSD cases account for 20-40% of congenital heart disease.Perimembranous VSD is the most common type, accounting for as many as 50% of VSD casesidentified in most surgical or autopsy series.

Race-, sex-, and age-related demographics

Inheritance patterns of different VSDs vary widely by race. Perimembranous VSD has no knownrace predilection. Defects located in a subpulmonary position, such as supracristal defects , aremore common in the Asian population. VSDs are slightly more common in females than inmales.

Most perimembranous VSDs present clinically in the neonatal period secondary to a murmur.These defects, especially the smaller defects, are not typically suspected at birth and may not beidentified by auscultation until PVR begins to fall in the first few days to weeks of life. Large

perimembranous VSDs may not present until patients are aged 6-8 weeks, when decreased PVRallows significant left-to-right shunting and clinical signs and symptoms of CHF. VSDs may

present soon after birth if associated with significant additional congenital heart lesions or if theyoccur with an associated chromosomal anomaly or syndrome.

Prognosis

Children with small-to-moderate sized ventricular septal defects (VSDs) have an excellent prognosis; infants and children with large VSDs have a good prognosis. Optimal medical

management, with appropriate timing of surgical intervention, has the best outcome.

Morbidity and mortality

Morbidity and mortality are influenced by the number and size of VSDs, the degree of left-to-right shunting, the presence of associated congenital heart defects, the presence of associatednoncardiac defects and syndromes, and age at repair of VSD.
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Perimembranous VSDs may spontaneously decrease in size and eventually close. (This oftenoccurs with a small defect.) Closure rates as high as 50% have been reported in some series, butcontinued follow-up care is warranted until documented VSD closure occurs.

Although patients with a small VSD have an excellent prognosis, small perimembranous VSDs

may lead to the development of aortic insufficiency.

For patients with moderate-sized VSD, defects may allow the development of voluminous left-to-right shunting in the first few months of life as PVR falls. Failure of medical management,with persistent evidence of CHF, is the primary indication for surgical closure of moderate-sizeddefects. Fewer than 25% of moderate-sized defects require surgical closure.

For patients with large muscular VSDs, surgical repair is indicated at any time during the firstyear of life if the infant fails to grow appropriately despite optimal medical management.Surgical risk and mortality for patients with large VSDs is higher in the first 2 months of life (10-20%) than after age 6 months (1-2%), although these figures have been decreasing. Elective

surgical closure of large VSDs should be planned within the first year of life to preventdevelopment of irreversible pulmonary vascular obstructive disease (ie, Eisenmenger syndrome).

History

Murmur

Most patients with small perimembranous ventricular septal defects (VSDs) are asymptomatic but come to medical attention because a systolic murmur is discovered. Patients with large,isolated perimembranous VSDs are typically asymptomatic in the newborn period.

Progression of symptoms

Typically, infants with large VSDs present with signs and symptoms of pulmonaryovercirculation or CHF at age 6-8 weeks or older, as PVR continues to fall and the degree of left-to-right shunting increases.

Signs and symptoms include poor feeding, decreased weight gain, tachypnea, tachycardia,sweating (especially with feeding), and lethargy.

Chromosomal anomalies

VSDs are the most common congenital heart lesion (20-30%) in infants with chromosomalanomalies or syndromes. These defects may be discovered in the first days of life whenadditional diagnostic evaluations are performed to exclude multiple congenital defects.

Physical Examination


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The size of the ventricular septal defect (VSD) and the degree of left-to-right shuntingsignificantly influence findings in a typical physical examination. The following may be foundwith small VSDs:

Normal vital signs with normal weight gain

Quiet precordium with normal apical impulse Normal first heart sound Narrowly split second heart sound; occasional accentuated pulmonary component Absent third heart sound Palpable thrill at the mid- to lower left sternal border (very small VSDs) Absent diastolic murmur with small VSDs

A grade II-VI/VI holosystolic murmur that widely radiates throughout the precordium is presentalong the left sternal border. The intensity of the murmur is usually inversely proportional to thesize of the defect, the left ventricular to right ventricular pressure gradient, and the degree ofleft-to-right shunting. In general, smaller defects produce louder murmurs. Systolic murmurs

from VSDs are usually holosystolic; they may occasionally sound crescendo or crescendo-decrescendo.

The following may be shown with large VSDs:

Poor growth and weight gain Symptoms of CHF, including tachypnea, tachycardia, sweating, and pallor Hyperdynamic precordium with or without precordial bulge due to underlying

cardiomegaly. Abnormal apical impulse with or without right ventricular tap; a thrill is uncommon Normal first heart sound and a narrowly split second heart sound with occasional loud

pulmonary component A loud holosystolic murmur with wide precordial radiation maximal at the left mid-sternal border

A prominent third heart sound that produces a gallop rhythm at the apex. A mid-diastolic flow rumble at the cardiac apex, caused by a significant (at least 2:1

ratio) left-to-right shunt with excessive flow across a normal mitral annulus

Differential Diagnoses

Aortic Stenosis, Subaortic Double Outlet Right Ventricle, Normally Related Great Arteries Double-Chambered Right Ventricle Pulmonary Stenosis, Infundibular Ventricular Septal Defect, Muscular Ventricular Septal Defect, Supracristal

Approach Considerations
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For children with small ventricular septal defects (VSDs), no specific laboratory blood tests areindicated. Occasionally, in the evaluation of children with symptomatic large VSD, brainnatriuretic peptide (BNP) is measured as a marker of congestive heart failure (CHF) severity.

Children who are maintained on diuretics and angiotensin-converting enzyme (ACE) inhibitors

must have their electrolyte levels periodically measured.

Electrocardiography

Electrocardiographic findings vary depending on the VSD size and the degree of intracardiacshunting. Patients with small VSDs have normal ECG findings; large VSDs show left ventricularhypertrophy (LVH) (ie, volume overload), right ventricular hypertrophy (RVH) (ie, pressureoverload), and left atrial enlargement.

Imaging Studies

Chest radiography

Small ventricular septal defects (VSDs) show normal cardiac size and normal pulmonaryvascularity.

Large VSDs demonstrate cardiac enlargement and increased pulmonary vascular markings proportional to the size of left-to-right shunt, left atrial and left ventricular enlargement, posteriordisplacement of the left ventricular apex, and prominence of the main pulmonary artery segment.

Two-dimensional echocardiography and Doppler ultrasonography

Echocardiography is the most reliable noninvasive modality to identify the presence, size,number, and location of the VSD. Perimembranous VSDs are readily identified from thesubcostal short- and long-axis planes, the apical 4-chamber, parasternal long axis, and

parasternal short-axis scan planes.

Small VSDs (defined as VSD dimension less than half the size of the aortic annulus diameter)are usually isolated defects with otherwise normal cardiac anatomy and function. Large VSDs(defined as defect size equal to the diameter of the aortic annulus) typically have left atrial andleft ventricular dilation with normal left ventricular systolic function. Dilation of the main and

branch pulmonary arteries also is common.

Doppler echocardiography can be used to predict the intracardiac pressure gradient from the leftventricle to the right ventricle using the continuous wave Doppler tracing (modified Bernoulliequation = 4 [velocity squared]). If the systolic systemic pressure is known, in the absence ofaortic outflow obstruction, right ventricle and pulmonary artery (in the absence of rightventricular outflow obstruction) systolic pressures can be predicted by subtracting the gradient

between the ventricles from the aortic systolic blood pressure.


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Color Doppler is useful to determine VSD location and size as well as the degree of intracardiacshunting.

Echocardiography is also essential to rule out other commonly associated congenital heartlesions, including atrial septal defects, patent ductus arteriosus, pulmonary valve stenosis, and

complex congenital heart disease with an associated VSD.

Three-dimensional echocardiography

Real-time 3-dimensional echocardiography (RT3DE) can be used to characterize the ventricularseptum. RT3DE allows accurate determination of VSD size, shape, and location. The shortacquisition time and acceptable reconstruction time make this technique clinically applicable .[3]

Magnetic resonance imaging

Cardiac magnetic resonance imaging (MRI) is a useful adjunct in the evaluation of large

muscular VSDs. Black blood imaging at end-diastole reliably shows the anatomy of theventricular septum, ventricular chambers, and great vessels. Bright blood gradient-echo dynamicimages are useful for evaluating the anatomy in all segments of the cardiac cycle. Tiny muscularVSDs are not well seen using cardiac MRI.

Flow-sensitive phase contrast imaging is the criterion standard for determining the direction andmagnitude of shunting. It can alleviate the requirement for cardiac catheterization in some cases.

Cardiac Catheterization and Angiography

Cardiac catheterization

Routine diagnostic cardiac catheterization is no longer required for perimembranous ventricularseptal defects (VSDs). However, older children and adults with a large VSD usually requirecardiac catheterization prior to surgical closure to assess PVR.

Indications for cardiac catheterization in patients with VSD include inadequate noninvasiveechocardiographic assessment of the size, number, or location of the VSDs, as well ascomplicated associated anatomy.

Another indication is the requirement for additional hemodynamic data prior to medicalmanagement or surgical repair (eg, determination of PVR and its reactivity, quantitation of left-to-right shunting, exclusion of associated congenital heart defects).

Angiography

When angiography is employed, membranous VSDs are best demonstrated in the long axialoblique orientation.


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Surgical Intervention

Surgical repair is the most common intervention currently performed. Surgery is indicated in patients with progressive aortic insufficiency or greater than trivial insufficiency at the time ofinitial presentation.

Surgical repair of an isolated large ventricular septal defect (VSD) involves closure of the defectwith a Gore-Tex patch.

Surgical intervention in younger infants, especially those younger than 1 month, is associatedwith an increased risk of mortality (historically as high as 10%, although currently much lower).Surgical mortality is now very low (approximately 1%) in patients older than 6 months with anisolated perimembranous VSD. New surgical approaches using smaller incisions have proveneffective in VSD closure.

Approach ConsiderationsSmall perimembranous ventricular septal defects (VSDs) have a spontaneous closure rate of ashigh as 50% within the first 2 years of life and often do not require medical or surgicalmanagement.

Larger defects may not close but often become smaller with time. Medical therapy may berequired with large membranous VSDs due to excessive left-to-right shunting and CHF. Therapyis directed at alleviating the symptoms of pulmonary overcirculation. Treatment typicallyincludes increased-calorie feedings, diuretics, and, sometimes, an ACE inhibitor.

Diuretic therapy with furosemide is used to lessen volume overload. Significant potassiumwasting may warrant the addition of spironolactone or potassium supplementation.

The use of afterload reduction to improve systemic-pulmonary flow ratios may be beneficial inselected cases. ACE inhibitors also inhibit the tissue-based renin-angiotensin system, preventingdeleterious remodeling. Be aware that ACE inhibitors have a potassium-sparing effect. Whenthese are used, spironolactone or supplemental potassium should be avoided or judiciously used.

Surgical indications

Failure of medical management to alleviate symptoms in the first 6 months of life requires

intervention. Growth failure despite optimal medical therapy and maximized calorie intake is themost important evidence of failure of medical therapy. Intervention in VSD is either by surgeryor cardiac catheterization .[4] Very large left-to-right shunts are usually electively repaired withinthe first year of life.

Severe CHF requiring hospitalization indicates the need for early intervention for VSD closure.Surgical closure is also required for any size of VSD with the development of progressive aorticvalve regurgitation.


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Elevated pulmonary arteriolar resistance of more than 12 Wood units that does not decrease withoxygen or selective pulmonary vasodilator therapy may be regarded as inoperable.

Diet and activity

Patients with significant CHF may require caloric supplementation with fortified formula or breast milk.

Patients with small perimembranous VSDs have no activity restrictions. Patients with moderate-to-large perimembranous defects and significant symptomatology limit their own exerciseactivity levels until the defect is repaired. Patients with repaired VSDs and no residual cardiacsequelae have no activity restrictions.

Transfer

Patients with large or multiple VSDs may be transferred to a tertiary care center for further

diagnostic evaluation or surgical intervention.

Consultations

Consultations with the following specialists may be indicated:

Pediatric cardiologist Pediatric cardiothoracic surgeon, if surgery is needed

Cardiac Catheterization and Hybrid Procedures

Devices are now available for the closure of perimembranous ventricular septal defects(VSDs) .[5, 6, 7, 8, 9] VSD closure devices typically have 2 asymmetrical, opposing discs (one for theright ventricular side and one for the left ventricular side), which are released duringcatheterization under fluoroscopic and transesophageal echocardiographic guidance to occludethe defect.

These devices can be placed percutaneously in the cardiac catheterization laboratory or in theoperating room during a "hybrid procedure." These procedures are slightly more complicatedthan closure of muscular VSDs because of the asymmetry of the device, the proximity to theaortic valve, and the presence of conduction tissue very near the defect.

Hybrid procedures may involve inserting the device through a very small incision in the free wallof the right ventricle.

Ongoing investigational trials are currently being performed to assess indications for andoutcomes in VSD closure with these devices.


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One report noted effective closure in children using the Amplatzer asymmetrical perimembranous occluder in 35 patients with a median age of 4.5 years .[10, 8] The defects were 3-8 mm in size, and the size of the occluder varied from 4-12 mm. After 2.5 years, the rate ofcomplete closure was 91%. Two further studies concluded that the procedure is safe, butwarrants further study and requires great skill in cases with small infants .[8, 11]

Complications in the study included residual shunting that required surgical closure of the defectsubsequent to the insertion of the device and persistent regurgitation across the tricuspid or aorticvalve related to the occluder. Conduction abnormalities related to the procedure occurred in 20%of the patients. The abnormalities were permanent in all but one of these patients.

Outpatient Care and Monitoring

Routine inpatient monitoring of infants and children with small perimembranous ventricularseptal defects (VSDs) is not necessary.

Manage patients with large VSDs and no CHF on an outpatient basis. Mild to moderatecongestive heart failure (CHF) secondary to large left-to-right shunting caused by a VSD is alsomanaged on an outpatient basis.

Small perimembranous VSDs have a 50% spontaneous closure rate. Perform serial follow-upcare until the VSD closes.

Manage moderately-sized VSDs on an outpatient basis by monitoring for evidence of a reductionin size or a spontaneous closure. Assess patient growth and evaluate the need for electivesurgical closure.

For routine perimembranous VSDs, antibiotics for the prevention of bacterial endocarditis are nolonger recommended by the American Heart Association .[12] A modest risk of endocarditis is stillobserved; thus, the importance of vigilant oral hygiene should be reinforced.

Medication Summary

Diuretics are now the mainstay of medical therapy for infants and children with large ventricularseptal defects (VSDs), large left-to-right shunts, and evidence of CHF. Current debate is ongoingconcerning the use of digoxin. In certain situations, the addition of afterload reduction may also

be beneficial. Hemoglobin levels should be normal.

As previously mentioned, be aware that ACE inhibitors have a potassium-sparing effect; whenthese are used, spironolactone or supplemental potassium should be avoided or judiciously used.

Diuretics

Class Summary


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These agents relieve ventricular volume load and peripheral and pulmonary congestion.

View full drug information

Furosemide (Lasix)

Furosemide increases the excretion of water by interfering with the chloride-binding cotransportsystem, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henleand distal renal tubule.

Spironolactone (Aldactone)

Spironolactone is used for the management of edema resulting from excessive aldosteroneexcretion. It competes with aldosterone for receptor sites in the distal renal tubules, increasingwater excretion while retaining potassium and hydrogen ions.

Afterload Reducers

Class Summary

These drugs decrease systemic afterload and may decrease left-to-right shunting through a largeventricular septal defect (VSD). They are used to improve preoperative or postoperative cardiac

output, reducing systemic vascular resistance and increasing systemic blood flow resulting frommyocardial dysfunction.


Enalapril (Vasotec)

Enalapril is a competitive inhibitor of ACE; it reduces angiotensin II levels, decreasingaldosterone secretion.


Captopril
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Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor,resulting in lower aldosterone secretion.

Inotropic Agents

Class Summary

These agents augment ventricular contractility. Positive inotropic agents increase the force ofcontraction of the myocardium and are used to treat acute and chronic CHF. Some may alsoincrease or decrease the heart rate (ie, positive or negative chronotropic agents), providevasodilatation, or improve myocardial relaxation. These additional properties influence thechoice of drug for specific circumstances. Cardiac glycosides are used predominantly for theirinotropic effects.


Digoxin (Lanoxin)

Digoxin is a cardiac glycoside with direct inotropic effects; it also has indirect effects on thecardiovascular system. Digoxin inhibits sodium- and potassium-activated adenosinetriphosphatase (NaK-ATPase), which causes intracellular calcium in the sarcoplasmic reticulumof cardiac cells to increase.
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