Third-Degree Atrioventricular Block Medication

Updated: Dec 31, 2015
  • Author: Adam S Budzikowski, MD, PhD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Medication

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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