Coarctation of the Aorta Medication

Updated: Nov 20, 2018
  • Author: Syamasundar Rao Patnana, MD; Chief Editor: Stuart Berger, MD  more...
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Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications of coarctation of the aorta (CoA).

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Prostaglandins

Class Summary

Alprostadil (PGE1) promotes dilatation of the ductus arteriosus in infants with ductal-dependent cardiac abnormalities.

Alprostadil IV (Prostin VR Pediatric Injection)

Identical to the naturally occurring prostaglandin E1 (PGE1) and possesses various pharmacologic effects, including vasodilation and inhibition of platelet aggregation.

First-line medication used as palliative therapy to temporarily maintain patency of the ductus arteriosus before surgery. Beneficial in infants with congenital defects that restrict pulmonary or systemic blood flow and in patients who depend on a PDA for adequate oxygenation and lower-body perfusion. Produces vasodilation and increases cardiac output. Each 1-mL ampule contains 500 mcg/mL.

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Inotropic agents

Class Summary

These agents are used to stimulate alpha-receptor and beta-receptors in the heart and vascular bed. 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.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. Hemodynamic effects depend on the dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation are produced by higher doses.

Positive inotropic agent at 2-10 mcg that can lead to tachycardia, ischemia, and dysrhythmias. Doses >10 mcg cause vasoconstriction, which increases afterload.

Dobutamine (Dobutrex)

Produces vasodilation and increases the inotropic state. At higher doses, may cause increased heart rate, thereby exacerbating myocardial ischemia. Strong inotropic agent with minimal chronotropic effect and no vasoconstriction.

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Cardiac glycosides

Class Summary

These medications improve ventricular systolic function by increasing the calcium supply available for myocyte contraction.

Digoxin (Lanoxin)

This form inhibits the sodium-potassium ATPase pump in cardiac myocytes.

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Diuretic agents

Class Summary

These agents promote excretion of water and electrolytes by the kidneys. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention have resulted in edema or ascites. Generally includes a loop diuretic that inhibits sodium chloride reabsorption in the ascending loop of Henle.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium chloride reabsorption in the ascending loop of Henle and distal renal tubules. Dose must be individualized to patient. Depending on response, administer at increments no sooner than 6-8 h after the previous dose, until desired diuresis occurs.

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Beta-adrenergic blocking agents

Class Summary

These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation. Preoperative hypertension can be treated effectively with beta-blockers.

Metoprolol (Lopressor)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG. When considering conversion from IV to PO dosage forms, use ratio of 2.5 mg PO to 1 mg IV metoprolol.

Esmolol (Brevibloc)

Ultra–short-acting beta2-blocker. Particularly useful in patients with labile arterial pressure, especially if surgery is planned, because it can be discontinued abruptly, if necessary. May be useful as a means to test beta-blocker safety and tolerance in patients with history of obstructive pulmonary disease who are at uncertain risk for bronchospasm from beta-blockers. Elimination half-life is 9 min.

Labetalol (Normodyne, Trandate)

Blocks alpha-aderenergic, beta1-aderenergic, and beta2-aderenergic receptor sites, decreasing BP.

Propranolol (Inderal, Betachron E-R)

Class II antiarrhythmic nonselective beta-adrenergic receptor blocker. Has membrane-stabilizing activity and decreases automaticity of contractions. Not suitable for emergency treatment of hypertension.

Atenolol (Tenormin)

Selectively blocks beta1-receptors with little or no effect on beta2-receptors.

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Angiotensin-converting enzyme (ACE) inhibitors

Class Summary

These agents reduce afterload and decrease myocardial remodeling that worsens chronic heart failure. May be added if hypertension persists despite beta-blocker therapy and no residual arch obstruction is noted.

Captopril (Capoten)

ACE inhibitors decrease the production of angiotensin II, a potent vasoconstrictor, resulting in peripheral vasodilatation and afterload reduction, improved myocardial performance, and theoretically reduced atrioventricular and semilunar valve insufficiency.

Enalapril (Vasotec)

Competitive ACE inhibitor with prolonged duration of action with oral administration.

Reduces angiotensin II levels, reducing aldosterone secretion.

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Vasodilators

Class Summary

Postoperative hypertension can be treated short-term with vasodilators, which reduce SVR, allowing more forward flow, thus improving cardiac output.

Nitroprusside (Nitropress)

Directly acting vasodilator. Exerts its effect on both arterial and venous circulation. Causes reflex tachycardia, small decrease in cardiac output, and decreases total peripheral resistance and cardiac and stroke index.

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