Truncus Arteriosus Medication

  • Author: Doff B McElhinney, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: May 18, 2012
 

Medication Summary

Pharmacologic therapy in patients with truncus arteriosus depends on various factors, including clinical status, associated lesions, and where in the course of management (eg, preoperative, early postoperative) the patient is when drug therapy is provided. The major classes of cardiac drugs administered to patients with truncus arteriosus include diuretics, digoxin, afterload reducing agents, inotropic medications, and antiarrhythmics if necessary. Consultation with a cardiologist is imperative before beginning, changing, or discontinuing cardiac medications in these patients.

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Inotropic agents

Class Summary

These agents provide inotropic and chronotropic support in the early postoperative period, when postoperative myocardial edema and ischemia-reperfusion injury may result in varying degrees of residual ventricular dysfunction. Also used at low doses to optimize renal perfusion to facilitate diuresis.

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Dopamine (Intropin)

 

Stimulates adrenergic and dopaminergic receptors, with a predominant dopaminergic effect at low doses, beta-adrenergic and dopaminergic effects at intermediate doses, and primarily alpha-adrenergic effects at high doses.

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Diuretic agents

Class Summary

These medications are used to mobilize edema in the early postoperative period and facilitate fluid homeostasis. They are also used for treatment of hypertension.

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Furosemide (Lasix)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

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Cardiac glycoside, antiarrhythmic

Class Summary

These agents are used to increase myocardial contractility, to slow atrioventricular node conduction time, and to potentiate the effects of furosemide.

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Digoxin (Lanoxin, Lanoxicaps)

 

Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

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ACE inhibitor, afterload reducing agent

Class Summary

These agents are used to decrease systemic vascular resistance, which is beneficial in patients with hypertension, impaired ventricular function, or aortic/truncal valve regurgitation.

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Captopril (Capoten)

 

Inhibits activity of the angiotensin-converting enzyme, preventing conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor. Decreased levels of angiotensin II lead to increased plasma renin activity and decreased circulating aldosterone.

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Contributor Information and Disclosures
Author

Doff B McElhinney, MD  Assistant Professor of Pediatrics, Harvard Medical School; Associate in Cardiology, Department of Cardiology, Children's Hospital of Boston

Doff B McElhinney, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology

Disclosure: Nothing to disclose.

Coauthor(s)

Gil Wernovsky, MD, FACC, FAAP  Professor, Department of Pediatrics, University of Pennsylvania, Children's Hospital of Philadelphia

Gil Wernovsky, MD, FACC, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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.

Ameeta Martin, MD  Clinical Associate Professor, Department of Pediatric Cardiology, University of Nebraska College of Medicine

Ameeta Martin, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

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.

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Anatomic subtypes of truncus arteriosus (TA), according to the classification systems of both Collett and Edwards (I, II, III) and the Van Praaghs (A1, A2, A3, A4).
Pathologic specimen with truncus arteriosus (TA), viewed through the opened right ventricle and truncal valve. The common trunk (CT) can be seen giving off the ascending aorta (AA) as well as the left (LPA) and right (RPA) pulmonary arteries. The truncal valve straddles the ventricular septal defect (VSD). The tricuspid valve (TV) also is labeled. Photograph courtesy of Robert H. Anderson, MD.
Pathologic specimen with truncus arteriosus (TA) and interruption of the aortic arch between the left (L) common carotid (CCA) and subclavian (SCA) arteries, viewed from the anterior aspect. The common trunk (CT) is seen arising from the ventricular mass, including the right ventricular (RV) infundibulum. Pulmonary arteries arise as a single trunk from the leftward aspect of the common trunk, which then divides into left and right branches (not shown) and the arterial duct (DA), which continues into the descending aorta, from which the left subclavian artery arises. The ascending aorta (AA), which supplies only the right (R) and left common carotid arteries (the right subclavian artery, which arises anomalously as the last brachiocephalic branch, is not shown), continues from the rightward aspect of the common trunk and is much smaller than in patients without an interrupted arch. RA=right atrial appendage. Photograph courtesy of Robert H. Anderson, MD.
Echocardiographic images of truncus arteriosus (TA). The top image is from the subcostal coronal window (SC COR) and shows the common trunk (TR) arising from the left ventricle (LV), overriding the interventricular septum. The common trunk branches into the pulmonary trunk and the ascending aorta (AO). The left pulmonary artery (LPA) may be seen branching from the pulmonary trunk. RA=right atrium; RPA=right pulmonary artery. In the bottom image, which is from the suprasternal notch sagittal window, the truncal origin and course of the pulmonary trunk and left pulmonary artery can be appreciated. DAO=descending aorta; IV=innominate vein; LA=left atrium.
 
 
 
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