Pediatric Unbalanced Atrioventricular Septal Defects Medication

Updated: Jan 04, 2016
  • Author: Mark A Law, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
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Medication Summary

No specific or recommended drug therapy is available for unbalanced atrioventricular (AV) septal defects. If evidence of pulmonary overcirculation is present, management of congestive heart failure (CHF) with digoxin, diuretics, and ACE inhibitors may be indicated. ACE inhibitors may also be indicated for atrioventricular valve (AVV) regurgitation.


Cardiac glycosides

Class Summary

These agents theoretically provide a positive inotropic effect. They are used to treat acute and chronic CHF.

Digoxin (Lanoxin)

Frequently used cardiac glycoside that inhibits the sarcolemmal sodium-potassium ATPase, leading to an increase in intracellular calcium concentration and increased myocardial contractility.


Loop diuretics

Class Summary

These agents inhibit electrolyte reabsorption in the ascending loop of Henle, thereby promoting diuresis. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention has resulted in edema or ascites.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system that inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal tubule.


ACE inhibitors

Class Summary

ACE inhibitors are beneficial in all stages of chronic heart failure. Pharmacologic effects result in decreased systemic vascular resistance, reducing blood pressure, preload, and afterload.

Captopril (Capoten)

Inhibits activity of ACE, thereby preventing conversion of angiotensin I to angiotensin II (a potent vasoconstrictor). Decreased levels of angiotensin II lead to increased plasma renin levels and decreased aldosterone levels.

Enalapril (Vasotec)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Helps control blood pressure and proteinuria. Decreases pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance. Has favorable clinical effect when administered over a long period. Helps prevent potassium loss in distal tubules. The body conserves potassium; thus, less oral potassium supplementation needed.

Patients who develop a cough, angioedema, bronchospasm, or other hypersensitivity reactions after starting ACEIs should be switched to an angiotensin-receptor blocker.