Perimembranous Ventricular Septal Defect Medication

  • Author: Michael D Taylor, MD, PhD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Nov 1, 2011
 

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 evidence 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.

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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.

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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.

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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.

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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, and Society for Cardiovascular Magnetic Resonance

Disclosure: Nothing to disclose.

Coauthor(s)

Benjamin W Eidem, MD, FACC, FASE, FAAP  Associate Professor, Divisions of Pediatric Cardiology and Cardiovascular Diseases, Department of Pediatrics, Mayo Clinic College of Medicine

Benjamin W Eidem, MD, FACC, FASE, FAAP 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, and Society of Pediatric Echocardiography

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.

Additional Contributors

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
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  8. 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. Oct 9 2007;116(15):1736-54. [Medline].

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