Ventricular Septal Defects Medication

  • Author: Prema Ramaswamy, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Nov 1, 2011
 

Medication Summary

Medications used in the management of ventricular septal defects (VSDs) include diuretics, angiotensin-converting enzyme (ACE) inhibitors, and cardiac glycosides.

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Diuretics, Loop

Class Summary

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.

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Furosemide (Lasix)

 

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

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ACE Inhibitors

Class Summary

ACE inhibitors are used to treat congestive heart failure (CHF). They may be of use to treat systemic afterload.

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Captopril

 

Captopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, lowering aldosterone secretion. It can be useful in reducing systemic afterload.

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Enalapril (Vasotec)

 

Enalapril is considered a reasonable first drug of choice in this group because of its increased dosing interval (q12-24h). A competitive ACE inhibitor, it reduces angiotensin II levels, decreasing aldosterone secretion. Enalapril is available in a liquid suspension.

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Lisinopril (Prinivil, Zestril)

 

Lisinopril is considered a reasonable first drug of choice in this group because of its increased dosing interval (q12-24h). It 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

Cardiac glycosides 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 atrioventricular (AV) node; therefore, they have a negative chronotropic effect. Cardiac glycosides have similar pharmacologic effects but differ considerably 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.

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Digoxin (Lanoxin)

 

Digoxin is a cardiac glycoside with direct inotropic effects, in addition to indirect effects on the cardiovascular system. It acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions increase the activity of the carotid sinus nerve and enhance sympathetic withdrawal for any given increase in mean arterial pressure.

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Contributor Information and Disclosures
Author

Prema Ramaswamy, MD  Associate Professor of Clinical Pediatrics, State University of New York Downstate; Adjunct Assistant Clinical Professor of Pediatrics, St George's University School of Medicine; Co-Director of Pediatric Cardiology, Maimonides Medical Center, Lutheran Medical Center, and Coney Island Hospital

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)

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.

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

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.

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.

Viswanath Natesan, MD Staff Physician, Department of Internal Medicine, Lutheran Medical Center

Disclosure: Nothing to disclose.

Ashmitha Srinivasan Drexel University College of Medicine

Disclosure: Nothing to disclose.

Sharmila Srinivasan State University of New York Upstate Medical University

Disclosure: Nothing to disclose.

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, New York Academy of Sciences, Society for Pediatric Research,Texas Medical Association, and Texas Pediatric Society

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.

Additional Contributors

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.

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.

Viswanath Natesan, MD Staff Physician, Department of Internal Medicine, Lutheran Medical Center

Disclosure: Nothing to disclose.

Ashmitha Srinivasan Drexel University College of Medicine

Disclosure: Nothing to disclose.

Sharmila Srinivasan State University of New York Upstate Medical University

Disclosure: Nothing to disclose.

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, New York Academy of Sciences, Society for Pediatric Research,Texas Medical Association, and Texas Pediatric Society

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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A: Image shows a ventricular septum viewed from the right side. It has the following 4 components: inlet septum from the tricuspid annulus to the attachments of the tricuspid valve (I); trabecular septum from inlet to apex and up to the smooth-walled outlet (T); outlet septum, which extends to the pulmonary valve (O); and membranous septum. B: Anatomic positions of the defects are as follows: outlet defect (a); papillary muscle of the conus (b); perimembranous defect (c); marginal muscular defects (d); central muscular defects (e); inlet defect (f); and apical muscular defects (g).
Schematic representation of the location of various types of ventricular septal defects (VSDs) from the right ventricular aspect. A = Doubly committed subarterial ventricular septal defect; B = Perimembranous ventricular septal defect; C = Inlet or atrioventricular canal–type ventricular septal defect; D = Muscular ventricular septal defect.
Supracristal ventricular septal defect (VSD). Top image: Parasternal long-axis view shows the defect just below the aortic root. Middle image: The plane of sound is tilted to view the right ventricular outflow tract, and the defect is observed below the pulmonic valve. Bottom image: Parasternal short-axis view shows the ventricular septal defect between the aortic root (Ao) and the pulmonic valve (PV). LA = Left atrium; LV = Left ventricle; PA = Pulmonary artery; RA = Right atrium; RV = Right ventricle.
Echocardiogram of a child with a perimembranous ventricular septal defect (VSD). Note the defect at the 10 o'clock position in the parasternal short-axis view. AO = Aortic root; LA = Left atrium; LV = Left ventricle; PA = Pulmonary artery; RA = Right atrium; RV = Right ventricle.
Apical 4-chamber views. A: Image shows a large inlet defect. The defect is posterior and at the level of the atrioventricular valves. B: Image shows a small midmuscular ventricular septal defect. LA = Left atrium; LV = Left ventricle; PA = Pulmonary artery; RA = Right atrium; RV = Right ventricle.
Table. Aneuploid Syndromes Associated with Ventricular Septal Defect
SyndromeCCVM (%)Type of CCVM
Del 4q, 21, 3260Ventricular septal defect, atrial septal defect
Del 5p30-60Ventricular septal defect
Trisomy 1380Atrial septal defect, ventricular septal defect, TOF
Trisomy 18, Edwards syndrome100Ventricular septal defect, TOF, double-outlet right ventricle (DORV)
Trisomy 21, Down syndrome40-50Ventricular septal defect, atrioventricular canal (AVC)
Del 22q11, DiGeorge syndrome (single gene etiology, autosomal dominant)50Truncus arteriosus, TOF, ventricular septal defect
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