eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Ventricular Septal Defect, General Concepts: Treatment & Medication

Author: Prema Ramaswamy, MD, Co-director of Pediatric Cardiology, Maimonides Medical Center; Assistant Professor, Department of Pediatrics, Mount Sinai School of Medicine
Coauthor(s): Patturajah Anbumani, MD, MBBS, MS, MCh, Associate Medical Director, Best Medical Care; Former Associate Medical Director, Jeanes Hospital, Temple University Health System; Former Adjunct Clinical Assistant Professor, New York College of Osteopathic Medicine; Former Clinical Assistant Professor, Department of Medicine, State University of New York-Downstate; Kuruchi Srinivasan, MD, Consulting Staff, Department of Internal Medicine, Nazareth Hospital
Contributor Information and Disclosures

Updated: Feb 10, 2009

Treatment

Medical Care

Children with small ventricular septal defects (VSDs) are asymptomatic and have an excellent long-term prognosis. Neither medical therapy nor surgical therapy is indicated. Prophylactic antibiotic prophylaxis against endocarditis is no longer indicated. For more information, see Antibiotic Prophylactic Regimens for Endocarditis. Maintenance of good oral hygiene is of paramount importance in reducing the risk of endocarditis.

In children with moderate or large ventricular septal defects, a trial of medical therapy is indicated to manage symptomatic congestive heart failure (CHF) because many ventricular septal defects may become smaller with time. Therapies may include the following:

  • Increased caloric density of feedings to ensure adequate weight gain. Occasionally, oral feeds must be supplemented with tube feeds because a baby in CHF may be unable to consume adequate calories for appropriate weight gain.
  • Diuretics (eg, furosemide) may be used to relieve pulmonary congestion. Furosemide is usually given in a dosage of 1-3 mg/kg/d divided in 2 or 3 doses. Long-term furosemide treatment results in hypercalcemia and renal damage and electrolyte disturbances.
  • ACE inhibitors such as captopril and enalapril have proven helpful. The mechanism of action of these medications is to reduce both the systemic and pulmonary pressures (more so the latter), and this results in reducing the left to right shunt.
  • Digoxin (5-10 mcg/kg/d) may be indicated if diuresis and afterload reduction do not relieve adequately symptoms.

Surgical Care

Transcatheter closure

Muscular ventricular septal defects have been closed with transcatheter devices for the past 15 years. Although relatively common, perimembranous ventricular septal defects can be difficult to close percutaneously. Previous devices (eg, Rashkind or button devices) have been unsuccessful in attempts to close the ventricular septal defects because of the proximity of the defects to the aortic valve and potential aortic valve damage.

A newer device has undergone phase I trials in the United States. The device is an Amplatzer membranous ventricular septal defect occluder (AGA Medical Corporation; Golden Valley, Minnesota), which is an asymmetric, self-expandable, double-disk device, unlike the membranous occluder. Current recommendations are to use this device in older patients who weigh more than 8 kg and who have a subaortic rim of more than 2 mm.

Most procedures are performed with the patient under general anesthesia and with echocardiographic guidance. Reported complications have included aortic and tricuspid regurgitation, device embolization, complete heart block, transient left bundle-branch block, hemolysis, small residual shunts, and perforation.

In their phase I study, Fu et al reported 3 adverse events of complete heart block, perihepatic bleeding, and rupture of tricuspid valve chordae tendineae.9 In a previous article, they reported 2 cases of transient heart block that responded to high-dose steroids.10

More recent studies have shown that the Amplatzer membranous ventricular septal defect occluder resulted in excellent closure rates but had an unacceptably high rate of complete heart block.11,12

Surgical closure

The first operation described for the treatment of a ventricular septal defect was a palliative one and involved placing a restrictive band across the main PA.13 This was proposed since pulmonary vascular disease as a result of unimpeded flow to the lungs was recognized as a dreaded complication of a ventricular septal defect. This surgery was popular for about 2 decades because it was associated with low mortality and morbidity.

Lillehei and associates performed the first intracardiac repair was at the University of Minnesota in 1954 using a parent as an oxygenator and a pump in controlled cross-circulation.14 In the 1970s, the current techniques of hypothermia and cardiopulmonary bypass were first reported.15,16,17 At present, direct surgical repair by using cardiopulmonary bypass is the preferred surgical therapy in most centers. PA banding, part of a 2-stage procedure, is largely reserved for critically ill infants with multiple ventricular septal defect or for those with associated anomalies.

  • Indications for surgical repair
    • Uncontrolled CHF, including growth failure and recurrent respiratory infection is an indication for surgical repair. Neither the age nor the size of the patient is prohibitive in considering surgery.
    • Large, asymptomatic defects associated with elevated PA pressure are often repaired when infants are younger than 1 year, typically around age 6 years.
    • Surgical repair is indicated in older asymptomatic children with a normal pulmonary pressure if the pulmonary to systemic flow is greater than 2:1.
    • Prolapse of an aortic valve cusp is an indication for surgery despite the presence of only a small ventricular septal defect. Early repair may prevent progression of the aortic insufficiency.
  • Video-assisted cardioscopy
    • Short-term results of video-assisted cardioscopy for intraventricular repair of ventricular septal defect have led to its wide adoption as a means to reduce surgical trauma. Short-term results are excellent.
    • Long-term follow-up is necessary.
  • Approach
    • Most perimembranous and inlet defects are repaired by transatrial surgical approach.
    • Defects in the outlet septum are approached through the pulmonary valve.
    • Multiple muscular defects, especially near the apex, pose a difficult problem. Initial pulmonary banding or left ventricular (LV) approach through an apical left ventriculotomy and closing the defect by a single patch are the standard approaches.
    • Transcatheter therapy remains an experimental approach.
    • A hybrid operation is a joint procedure involving the interventional cardiologist and the cardiac surgeon who concomitantly optimize surgical management of complex congenital heart disease. This approach may be used for multiple ventricular septal defects where the perimembranous ventricular septal defect is repaired surgically and the muscular ventricular septal defects are closed using a transcatheter device.
  • Postoperative sequelae
    • A murmur of a residual ventricular septal defect is not infrequent. Selective use of intraoperative transesophageal echocardiography (TEE) to assess closure may be useful.
    • Decisions regarding reoperation are based on symptoms, left heart size, pulmonary pressure, and degree of shunting.
    • Right bundle branch block (RBBB) is common and may be caused by ventriculotomy or direct injury to the right bundle itself.
    • Complete heart block can rarely occur and is associated with late mortality.
    • LV dysfunction may occur after left ventriculotomy to close a muscular ventricular septal defect.
    • Ventricular arrhythmia can be a late problem.

Medication

Diuretics

Diuretics promote the excretion of water and electrolytes by the kidneys. They are used in the treatment of hypertension; heart failure; and hepatic, renal, or pulmonary disease when salt and water retention has resulted in edema or ascites.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized. Depending on response, administer in increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs. In infants, titrate in 1-mg/kg/dose increments until satisfactory effect achieved.

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states

Pediatric

1-3 mg/kg/d PO/IV divided bid/tid

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides (hearing loss of various degrees may occur); anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity possible when taken concurrently

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter; long-term treatment causes hypercalcemia and renal damage and electrolyte disturbances

ACE inhibitors

These drugs are used to treat CHF. They may be of use to treat systemic afterload.


Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, lowering aldosterone secretion. Can be useful in reducing systemic afterload.

Adult

6.25-12.5 mg PO tid; not to exceed 150 mg tid

Pediatric

0.1-0.3 mg/kg PO tid

Nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce hypotensive effects of captopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases captopril levels; probenecid may increase captopril levels; concurrent diuretics may enhance hypotensive effects of ACE inhibitors

Documented hypersensitivity; renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Unsafe in second and third trimester of pregnancy; safety for use during first trimester of pregnancy been established; caution in renal impairment, valvular stenosis, severe CHF, hyperkalemia, and concurrent use with potassium-sparing diuretics or NSAIDs

Cardiac glycosides

These drugs possess positive inotropic activity, which is mediated by inhibition of sodium-potassium adenosine triphosphatase (ATPase). The also reduce conductivity in the heart, particularly through the AV node; therefore, they have a negative chronotropic effect. Cardiac glycosides have similar pharmacologic effects but considerably differ in their speed of onset and duration of action. These agents are used to slow the heart rate in supraventricular arrhythmias, especially atrial fibrillation. They are also administered in chronic heart failure.


Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions increase activity of carotid sinus nerve and enhance sympathetic withdrawal for any given increase in mean arterial pressure.

Adult

0.125-0.375 mg PO qd

Pediatric

Total digitalizing dose:
Preterm infant: 20-30 mcg/kg PO
Term infant: 25-35 mcg/kg PO
1-5 years: 30-40 mcg/kg PO
5-10 years: 20-30 mcg/kg PO
Maintenance dose: 5-10 mcg/kg PO;
IV dose is 80% of PO dose

Medications that may increase levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, PO amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, PO colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in patients receiving digitalis; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are in the reference range; magnesium replacement must be started in patients with hypomagnesemia to prevent digitalis toxicity; patients with incomplete AV block may progress to complete block when treated; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

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References
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References

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Further Reading

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Keywords

ventricular septal defect, VSD, isolated ventriculoseptal defect, isolated ventricular defect, maladie de Roger, Eisenmenger complex, Eisenmenger's syndrome, Eisenmenger syndrome, tetralogy of Fallot, TOF), complete atrioventricular canal defects, transposition of great arteries, corrected transpositions, cyanosis, hypertension, perimembranous ventricular septal defect, perimembranous VSD, conal septal, infundibular, subpulmonic, subarterial, subarterial doubly committed, outlet, supracristal ventricular septal defect, polycythemia, congestive heart failure, CHF, infective endocarditis, cardiomegaly, tachycardia, congenital cardiovascular malformations, CCVM, gestational diabetes mellitus

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Contributor Information and Disclosures

Author

Prema Ramaswamy, MD, Co-director of Pediatric Cardiology, Maimonides Medical Center; Assistant Professor, Department of Pediatrics, Mount Sinai School of Medicine
Prema Ramaswamy, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology
Disclosure: Nothing to disclose.

Coauthor(s)

Patturajah Anbumani, MD, MBBS, MS, MCh, Associate Medical Director, Best Medical Care; Former Associate Medical Director, Jeanes Hospital, Temple University Health System; Former Adjunct Clinical Assistant Professor, New York College of Osteopathic Medicine; Former Clinical Assistant Professor, Department of Medicine, State University of New York-Downstate
Patturajah Anbumani, MD, MBBS, MS, MCh is a member of the following medical societies: American College of Physicians, American Medical Association, and American Medical Women's Association
Disclosure: Nothing to disclose.

Kuruchi Srinivasan, MD, Consulting Staff, Department of Internal Medicine, Nazareth Hospital
Kuruchi Srinivasan, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA, Professor, Departments of Pediatrics (Cardiology), Cardiovascular Sciences, and Molecular and Human Genetics, Baylor College of Medicine; Chief of Pediatric Cardiology, Foundation Chair in Pediatric Cardiac Research, Texas Children's Hospital
Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Cardiology, American College of Sports Medicine, American Heart Association, American Medical Association, American Society of Human Genetics, Cardiac Electrophysiology Society, Heart Rhythm Society, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Hugh D Allen, MD, Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine
Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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