Right Ventricular Infarction Medication

  • Author: Claudia Dima, MD; Chief Editor: Eric H Yang, MD   more...
 
Updated: Mar 29, 2011
 

Medication Summary

The goals of pharmacotherapy for right ventricular infarction are to reduce morbidity and prevent complications. Agents included in treatment are cardiovascular agents such as dobutamine and tissue plasminogen activators such as alteplase.[4, 8]

In addition, agents such as levosimendan (Simdax), a calcium sensitizer, have been developed for hospitalized patients with acutely decompensated heart failure. Levosimendan is not available in the United States and is only approved in Europe.

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Inotropic Agents

Class Summary

Inotropic therapy is indicated for right ventricular failure when cardiogenic shock persists after right ventricular end-diastolic pressure has been optimized. Inotropes should be used until more data are available. Dobutamine is an inotropic agent used to improve right ventricular contractility and maintain cardiac output.

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Dobutamine (Dobutrex)

 

Dobutamine produces vasodilation and increases the inotropic state. At higher dosages, this agent may cause increased heart rate, exacerbating myocardial ischemia.

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Milrinone

 

Milrinone is a bi-pyridine positive inotrope and vasodilator with little chronotropic activity. It is different in mode of action from both digitalis glycosides and catecholamines. It selectively inhibits phosphodiesterase type III (PDE III) in cardiac and smooth vascular muscle, resulting in reduced afterload, reduced preload, and increased inotropy.

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Tissue Plasminogen Activators

Class Summary

Tissue plasminogen activators bind to fibrin and convert plasminogen to plasmin, which in turn initiates local fibrinolysis with limited systemic proteolysis. Thrombolytic therapy may contribute to an early survival benefit in patients presenting within 6 hours of onset of onset of inferior wall myocardial infarction with right ventricular involvement diagnosed by ECG or other noninvasive criteria.

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Alteplase (Activase)

 

Alteplase is a tissue plasminogen activator used in the management of acute myocardial infarction, acute ischemic stroke, and pulmonary embolism. Heparin or aspirin may be administered with and after alteplase infusions to reduce the risk of rethrombosis. The safety and efficacy of concomitant administration of heparin or aspirin during the first 24 hours after symptom onset have not been investigated.

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Reteplase (Retavase)

 

Reteplase is a recombinant plasminogen activator that forms plasmin after facilitating cleavage of endogenous plasminogen. It is used in the management of acute myocardial infarction. Heparin or aspirin may be administered with and after reteplase infusions.

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Adrenergic Agonists

Class Summary

Adrenergic agonists stimulate beta- and alpha-adrenergic receptors, causing increased contractility and heart rate, as well as vasoconstriction. These actions increase systemic blood pressure and coronary blood flow.

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Norepinephrine (Levophed)

 

Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. It increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia.

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Antidiuretic Hormone Analogs

Class Summary

Antidiuretic hormone analogs increase cyclic adenosine monophosphate (cAMP), increasing water permeability at the renal tubules. An example of this analog is vasopressin, which is a direct vasoconstrictor without inotropic or chronotropic effects.

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Vasopressin (Pitressin)

 

Vasopressin increases water resorption at the distal renal tubular epithelium (ADH effect). It promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). Vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.

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Contributor Information and Disclosures
Author

Claudia Dima, MD  Fellow in Interventional Cardiology, Department of Cardiology, Banner Good Samaritan Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

David L Coven, MD, PhD  Assistant Professor of Medicine, Columbia University College of Physicians and Surgeons; Attending Physician in Interventional Cardiology, St Luke's-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Kenneth B Desser, MD  Clinical Professor, Director of Cardiology Fellowship, Banner Good Samaritan Medical Center, Phoenix, Arizona

Disclosure: Nothing to disclose.

Ashish Pershad, MD  Consulting Staff, Heart and Vascular Center of Arizona

Ashish Pershad, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

George A Stouffer III, MD  Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Chief Editor

Eric H Yang, MD  Associate Professor of Medicine, Director of Interventional Cardiology Fellowship Program, Henry Ford Hospital

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Rex C Liu, MD, to the development and writing of the source article.

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Table. Sensitivity and Specificity of More Than 1 mm of ST-Segment Elevation in V1, V3 R, and V4 R
Leads Sensitivity (%) Specificity (%)
V12892
V3 R6997
V4 R9395
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