Third-Degree Atrioventricular Block Medication

  • Author: Adam S Budzikowski, MD, PhD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Sep 16, 2011
 

Medication Summary

Common drugs that induce atrioventricular (AV) block include beta-blockers, calcium channel blockers, antiarrhythmics, and digoxin. Withdrawal of offending drugs is the first treatment for heart block. Patients with block at the level of the atrioventricular node (AVN), in the absence of ischemia, can benefit from sympathomimetic agents or vagolytic agents.

Medications that may be used in the management of third-degree AV block (complete heart block) include sympathomimetic or vagolytic agents, catecholamines, and antidotes.

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Sympathomimetic agents or vagolytic agents

Class Summary

Sympathomimetic or vagolytic agents improve conduction through the AVN by reducing vagal tone via muscarinic receptor blockade. They increase heart rate through their vagolytic effects, causing an increase in cardiac output.

Atropine (AtroPen)

 

Atropine is an antimuscarinic agent that enhances sinus node automaticity. It may enhance conduction and/or improve the rate of junctional escape. In addition, it blocks the effects of acetylcholine at the AVN, thereby decreasing the refractory time and speeding conduction through the AVN. At inefficient doses, atropine can have paradoxical effects, further slowing the heart rate (HR).

Isoproterenol hydrochloride (Isuprel)

 

Isoproterenol is a synthetic sympathomimetic acting directly on beta-receptors. It should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged. Cardiac ischemia or a high cardiac risk profile suggesting possible coronary artery disease is a contraindication to its use. Telemetry monitoring should always accompany the use of this agent because of the risks of proarrhythmia.

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Catecholamines

Class Summary

Catecholamines improve hemodynamics by acting on the beta-adrenergic receptors to increase the HR and contractility and by acting on the alpha-adrenergic receptors to increase the systemic vascular resistance.

Dopamine

 

Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1- and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion; it also stimulates release of norepinephrine.

In low doses (2-5 µg/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 µg/kg/min), it acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 µg/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure (BP).

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, HR, and vasoconstriction. It increases BP and afterload. The increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Norepinephrine is generally reserved for patients with severe hypotension (eg, systolic BP < 70 mm Hg) or hypotension unresponsive to other medication.

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Antidotes

Class Summary

Antidotes are used in select cases for patients with third-degree AV block secondary to digoxin toxicity. These patients should receive a digoxin-specific antidote.

Digoxin immune Fab (DigiFab)

 

Digoxin immune Fab is an immunoglobulin fragment with a specific and high affinity for both digoxin and digitoxin molecules. It removes digoxin or digitoxin molecules from tissue-binding sites. Each vial contains 40 mg of purified digoxin-specific antibody fragments, which will bind approximately 0.6 mg of digoxin or digitoxin.

The dose of the antidote depends on the total body load (TBL) of digoxin. The digoxin TBL can be estimated in the following 3 ways:

1. Estimate the quantity of digoxin ingested in the acute ingestion, and assume 80% bioavailability for digoxin or 100% for digitoxin (X mg ingested × 0.8 = TBL)

2. Obtain a serum digoxin concentration (in ng/mL) and multiply it by the patient's weight in kilograms. Divide the result by 100 [number of vials = (digoxin concentration) x (patient's weight) / 100]

3. Use an empiric dose based on average requirements for an acute or chronic overdose in an adult or child

If the quantity of ingestion cannot be estimated reliably, the antidote may be administered empirically (it is safest to use the largest calculated estimate). Alternatively, be prepared to increase dosing if resolution is incomplete.

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Contributor Information and Disclosures
Author

Adam S Budzikowski, MD, PhD  Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York Downstate Medical Center, University Hospital of Brooklyn

Adam S Budzikowski, MD, PhD is a member of the following medical societies: European Society of Cardiology, Heart Rhythm Society, and Polish Society of Cardiology

Disclosure: Boston Scientific Consulting fee Consulting; St. Jude Medical Honoraria Speaking and teaching; Zoll Honoraria Speaking and teaching

Coauthor(s)

Andrew C Corsello, MD  Consulting Staff, Department of Internal Medicine, Division of Cardiology, Cardiovascular Consultants of Maine, PA

Disclosure: Nothing to disclose.

James P Daubert, MD  Professor of Medicine, Cardiology Division, Duke University School of Medicine

James P Daubert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, and Heart Rhythm Society

Disclosure: Medtronic Equity interest None; Boston Scientific Honoraria Speaking and teaching; CV Therapeutics Consulting fee Consulting; Cryocor Consulting fee Consulting

Theodore J Gaeta, DO, MPH, FACEP  Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Michael D Levine, MD  Physician, Department of Medical Toxicology, Banner Good Samaritan Medical Center; Physician, Department of Emergency Medicine, Banner Thunderbird Medical Center

Michael D Levine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Abrar H Shah, MD  Clinical Assistant Professor, Department of Medicine, University of Rochester Medical Center; Consulting Staff, Department of Medicine (Cardiology), Strong Memorial Hospital, Geneva General Hospital; Consulting Staff, Department of Cardiology, Highland Hospital; Consulting Staff, Department of Cardiology and Electrophysiology, Park Ridge Hospital

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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

Brian Olshansky, MD  Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

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.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

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ECG before and after complete heart block at the AV nodal level.
Complete heart block with wide complex escape.
Electrocardiogram from patient in complete heart block.
 
 
 
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