Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Perimembranous Ventricular Septal Defect Medication

  • Author: Michael D Taylor, MD, PhD; Chief Editor: Howard S Weber, MD, FSCAI  more...
 
Updated: Nov 22, 2015
 

Medication Summary

Diuretics are now the mainstay of medical therapy for infants and children with large ventricular septal defects (VSDs), large left-to-right shunts, and symptoms of CHF. Current debate is ongoing concerning 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; when these are used, spironolactone or supplemental potassium should be avoided or judiciously used.

Next

Diuretics

Class Summary

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

Furosemide (Lasix)

 

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

Spironolactone (Aldactone)

 

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

Previous
Next

Afterload Reducers

Class Summary

These drugs decrease systemic afterload and may decrease left-to-right shunting through a large ventricular septal defect (VSD). They are used to improve preoperative or postoperative cardiac output, reducing systemic vascular resistance and increasing systemic blood flow resulting from myocardial dysfunction.

Enalapril (Vasotec)

 

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

Captopril

 

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

Previous
Next

Inotropic Agents

Class Summary

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

Digoxin (Lanoxin)

 

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

Previous
 
Contributor Information and Disclosures
Author

Michael D Taylor, MD, PhD Director, Advanced Imaging Innovation, Cincinnati Children's Hospital Medical Center; Assistant Professor, Department of Pediatrics, University of Cincinnati College of Medicine

Michael D Taylor, MD, PhD is a member of the following medical societies: American College of Cardiology, American Heart Association, Society for Cardiovascular Magnetic Resonance

Disclosure: Nothing to disclose.

Coauthor(s)

Benjamin W Eidem, MD, FACC, FASE Professor of Pediatrics and Medicine, Departments of Pediatrics and Medicine, Divisions of Pediatric Cardiology and Cardiovascular Diseases, Mayo Medical School

Benjamin W Eidem, MD, FACC, FASE is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Howard S Weber, MD, FSCAI Professor of Pediatrics, Section of Pediatric Cardiology, Pennsylvania State University College of Medicine; Director of Interventional Pediatric Cardiology, Penn State Hershey Children's Hospital

Howard S Weber, MD, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Received income in an amount equal to or greater than $250 from: St. Jude Medical.

Acknowledgements

Juan Carlos Alejos, MD Clinical Professor, Department of Pediatrics, Division of Cardiology, University of California, Los Angeles, David Geffen School of Medicine

Juan Carlos Alejos, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Medical Association, and International Society for Heart and Lung Transplantation

Disclosure: Actelion Honoraria Speaking and teaching

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.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References
  1. Williams LJ, Correa A, Rasmussen S. Maternal lifestyle factors and risk for ventricular septal defects. Birth Defects Res A Clin Mol Teratol. 2004 Feb. 70(2):59-64. [Medline].

  2. Oberlander TF, Warburton W, Misri S, Riggs W, Aghajanian J, Hertzman C. Major congenital malformations following prenatal exposure to serotonin reuptake inhibitors and benzodiazepines using population-based health data. Birth Defects Res B Dev Reprod Toxicol. 2008 Feb. 83(1):68-76. [Medline].

  3. Chen FL, Hsiung MC, Nanda N, Hsieh KS, Chou MC. Real time three-dimensional echocardiography in assessing ventricular septal defects: an echocardiographic-surgical correlative study. Echocardiography. 2006 Aug. 23(7):562-8. [Medline].

  4. Chessa M, Butera G, Negura D, et al. Transcatheter closure of congenital ventricular septal defects in adult: mid-term results and complications. Int J Cardiol. 2009 Mar 20. 133(1):70-3. [Medline].

  5. Fu YC, Bass J, Amin Z, et al. Transcatheter closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder: results of the U.S. phase I trial. J Am Coll Cardiol. 2006 Jan 17. 47(2):319-25. [Medline].

  6. Thanopoulos BD. Catheter closure of perimembranous/membranous ventricular septal defects using the Amplatzer occluder device. Pediatr Cardiol. 2005 Jul-Aug. 26(4):311-4. [Medline].

  7. Liu S, Chen F, Ding X, et al. Comparison of results and economic analysis of surgical and transcatheter closure of perimembranous ventricular septal defect. Eur J Cardiothorac Surg. 2012 Dec. 42(6):e157-62. [Medline].

  8. Lee SM, Song JY, Choi JY, et al. Transcatheter closure of perimembranous ventricular septal defect using amplatzer ductal occluder. Catheter Cardiovasc Interv. 2013 Dec 1. 82(7):1141-6. [Medline].

  9. Wang S, Zhuang Z, Zhang H, et al. Perventricular closure of perimembranous ventricular septal defects using the concentric occluder device. Pediatr Cardiol. 2014 Apr. 35(4):580-6. [Medline].

  10. Fischer G, Apostolopoulou SC, Rammos S, Schneider MB, Bjornstad PG, Kramer HH. The Amplatzer Membranous VSD Occluder and the vulnerability of the atrioventricular conduction system. Cardiol Young. 2007 Oct. 17(5):499-504. [Medline].

  11. Tzikas A, Ibrahim R, Velasco-Sanchez D, et al. Transcatheter closure of perimembranous ventricular septal defect with the Amplatzer(®) membranous VSD occluder 2: initial world experience and one-year follow-up. Catheter Cardiovasc Interv. 2014 Mar 1. 83(4):571-80. [Medline].

  12. Bai Y, Xu XD, Li CY, et al. Complete atrioventricular block after percutaneous device closure of perimembranous ventricular septal defect: A single-center experience on 1046 cases. Heart Rhythm. 2015 Oct. 12 (10):2132-40. [Medline].

  13. Hua N, Aquino P, Owada CY. Transcatheter closure of perimembranous ventricular septal defects with the Amplatzer Vascular Plug-II. Cardiol Young. 2015 Oct 26. 1-8. [Medline].

  14. Ebeid MR, Batlivala SP, Salazar JD, et al. Percutaneous closure of perimembranous ventricular septal defects using the second-generation Amplatzer vascular occluders. Am J Cardiol. 2015 Oct 17. [Medline].

  15. Omelchenko A, Gorbatykh Y, Voitov A, et al. Perventricular device closure of ventricular septal defects: results in patients less than 1 year of age†. Interact Cardiovasc Thorac Surg. 2015 Oct 13. [Medline].

  16. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007 Oct 9. 116(15):1736-54. [Medline].

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.