Syncope Medication

  • Author: Rumm Morag, MD, FACEP; Chief Editor: David FM Brown, MD   more...
 
Updated: Aug 11, 2011
 

Medication Summary

The goals of pharmacotherapy are to prevent complications and to reduce morbidity.

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Anticholinergics

Class Summary

These agents improve conduction through the atrioventricular node by reducing vagal tone via muscarinic receptor blockade. For patients with infranodal block, this therapy is ineffective.

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Atropine (Atropair, Isopto Atropine, Atropisol)

 

Anticholinergic (or parasympatholytic) drug that exerts its action by competitively inhibiting acetylcholine at muscarinic receptors on postganglionic smooth muscle. Can counteract rapidly heightened vagal tone in response to pathologic carotid sinus syndrome. Additionally, can reverse bradycardia and lessen degree of heart block when vagal activity is etiologic factor. Usual doses are used to reduce severe bradycardia and syncope associated with hyperactive carotid sinus reflex.

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Nutrient Supplements

Class Summary

Parenterally injected dextrose is used in patients unable to sustain adequate oral intake. Its direct oral absorption results in a rapid increase in blood glucose concentrations.

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Dextrose (D-Glucose)

 

Nutrient replenisher, serves to restore blood glucose levels. Each 100 mL of 5% dextrose contains 5 g of dextrose, whereas each 100 mL of 10% dextrose contains 10 g of dextrose.

Should be given only after demonstrated hypoglycemia.

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Benzodiazepines

Class Summary

CNS agents of the 1,4-benzodiazepine class exert their effects by binding at stereo-specific receptors in the CNS. Their exact mechanism of action has not been clearly elucidated. Benzodiazepines cause a dose-related CNS depression, which varies from mild sedation to hypnosis.

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Alprazolam (Xanax)

 

Indicated for treatment of anxiety and management of panic attacks. Following PO administration, absorbed readily. Peak concentrations in plasma occur 1-2 h following administration.

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Vasopressor

Class Summary

Midodrine forms an active metabolite, desglymidodrine, which is an alpha1-agonist that acts on receptors of the arteriolar and venous vasculature, producing an increase in vascular tone and elevation of BP. This drug has minimal beta effects and diffuses poorly across the blood-brain barrier.

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Midodrine HCl (ProAmatine)

 

Increases standing, sitting, and supine systolic and diastolic BP in patients with orthostatic hypotension of various etiologies. Standing systolic BP elevated by approximately 15-30 mm Hg at 1 h after 10-mg dose, with some effect persisting for 2-3 h. Has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure.

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Contributor Information and Disclosures
Author

Rumm Morag, MD, FACEP  Member of Salem Emergency Physician Services, PC (SEPS), Salem Hospital

Rumm Morag, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

David A Peak, MD  Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary

David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

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

Eddy S Lang, MDCM, CCFP(EM), CSPQ  Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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