Ventricular Septal Defects Medication

Updated: Dec 10, 2015
  • Author: Prema Ramaswamy, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
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Medication

Medication Summary

Medications used in the management of ventricular septal defects (VSDs) associated with evidence of left ventricular volume overload 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.

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.

Captopril

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

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.

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.

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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