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Heart Block, Third Degree: Treatment & Medication
Updated: Apr 13, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
- All patients should be rapidly transported to the nearest available facility, applying advanced life support (ACLS) with continuous cardiac monitoring, as per local protocols.
- For any symptomatic patient, transcutaneous pacing is the treatment of choice.
- In all patients, oxygen should be administered and intravenous access should be established.
- Maneuvers that are likely to increase vagal tone (eg, Valsalva maneuvers, painful stimuli) should be avoided.
- Atropine can be administered but should be given cautiously, because it is likely to be ineffective in a wide complex QRS rhythm and can be dangerous if the patient is having a concurrent MI.
Emergency Department Care
- Treatment in the ED should continue that already established in the prehospital setting, which includes administering oxygen, maintenance of an intravenous line, frequent monitoring of blood pressures, and continuous cardiac monitoring.
- AV nodal agents should be withheld, and anti-ischemic therapy should be started, when appropriate.
- Transcutaneous pacing pads should be applied and tested, if not already done so.
- As stated above, symptomatic patients in whom capture cannot be obtained with a transcutaneous pacemaker need urgent placement of a transvenous pacemaker. In asymptomatic patients in whom capture cannot be obtained, placement of a transvenous pacemaker is also indicated; the timing of this should be discussed with the consulting cardiologist.
- Hemodynamically stable patients in whom transcutaneous pacing can be successfully performed can go to a telemetry or intensive care unit at the discretion of the treating cardiologist.
- Hemodynamically unstable patients may be treated with atropine. However, if the rhythm is a wide complex escape rhythm, atropine is likely to be unsuccessful. In addition, caution should be taken when administering atropine to a patient with a suspected acute MI, as the resulting vagolysis leads to unopposed sympathetic stimulation, which can cause increased ventricular irritability and potentially dangerous ventricular arrhythmias. Similarly, isoproterenol may be attempted to accelerate a ventricular escape rhythm with a low probability for efficacy and the same concerns in patients with suspected acute MI.
- Hemodynamically unstable patients for whom timely cardiologic consultation is unavailable should undergo temporary transvenous pacemaker insertion in the ED.
- Arrange for permanent pacemaker insertion. Patients with complete heart block should be considered for permanent pacemaker insertion.5,6,7,8
Consultations
- Cardiologic consultation is indicated for all patients with third-degree AV block. The consultation is urgent in patients with concomitant acute MI, active myocardial ischemia, CHF, wide complex escape rhythm, or symptoms of hypoperfusion because patients in this group may require early placement of a permanent pacemaker or assistance may be needed if difficulty is encountered obtaining capture from an external or transvenous pacer.
Medication
The goal of therapy is to improve conduction through the AV node by reducing vagal tone via atropine-induced receptor blockade. However, this method is unlikely to be successful in wide-complex bradyarrhythmias, where the level of the block is below the level of the AV node, and this method should be given with caution in patients suspected of experiencing an MI. In addition, atropine is ineffective in patients with a denervated heart (eg, those patients who are post cardiac transplant).
Cases where complete heart block results from calcium channel blocker should be managed in the standard fashion for other etiologies of third-degree block (eg, pacemaker) but should also receive appropriate treatment for calcium channel blockers. This therapy includes the administration of IV fluids, calcium, glucagons, vasopressors, and high-dose insulin (hyperinsulinemic euglycemia [HIE] therapy). Further explanations of calcium channel blocker overdose can be found in the article on Toxicity, Calcium Channel Blocker. Overdoses on beta-blockers are managed a similar fashion as calcium channel blockers (see Toxicity, Beta-blocker, although HIE therapy for beta-blocker overdoses is less well established.
Anticholinergic agents
These agents improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade.
Atropine
Enhances sinus node automaticity. In addition, blocks effects of acetylcholine at AV node, thereby decreasing the refractory time and speeding conduction through AV node. At inefficient doses, atropine can have paradoxical effects, further slowing heart rate.
Adult
0.5 mg rapid IV push; for patients in PEA arrest, 1 mg can be administered; maximal IV dose is 0.04 mg/kg; atropine can also be administered via endotracheal tube, in which dose should be increased by 2-3 fold; when administered via endotracheal tube, absorption is less predictable when compared with IV administration
Pediatric
0.02 mg/kg IV push, with minimum of 0.1 mg; single dose should not exceed 0.5 mg in children, or 1 mg in adolescents; maximal total IV dose is 0.04 mg/kg; as stated in adult dosing, atropine can be administered via endotracheal tube
Coadministration with other anticholinergics have additive effects; pharmacologic effects of atenolol and digoxin may increase with atropine; antipsychotic effects of phenothiazines may decrease with this medication; tricyclic antidepressants with anticholinergic activity may increase effects of atropine
Documented hypersensitivity to atropine or belladonna alkaloids or related products; concomitant acute myocardial infarction/ischemia; thyrotoxicosis; narrow-angle glaucoma; congestive heart failure; tachycardia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in Down syndrome and/or children with brain damage to prevent hyperreactive response; caution also in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, hypertension, peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization
Catecholamines
These agents improve hemodynamics by acting on the beta-adrenergic receptors to increase the heart rate and contractility, and by acting on the alpha-adrenergic receptors to increase the systemic vascular resistance.
Dopamine (Intropin)
Naturally occurring endogenous catecholamine that stimulates beta1-and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion; stimulates release of norepinephrine.
In low doses (2-5 mcg/kg/min), acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 mcg/kg/min), acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 mcg/kg/min), acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise BP.
Adult
5-20 mcg/kg/min IV; at doses of 2-5 mcg/kg/min IV, dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, thereby causing vasodilation in these areas; in mid range doses (5-15 mcg/kg/min), dopamine acts preferentially on beta-adrenergic receptors to increase heart rate and contractility; at high doses (15-20 mcg/kg/min), dopamine acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise the blood pressure; medication should be given via continuous IV infusion; ideally, should be administered via a central venous line
Pediatric
Administer as in adults
MAO inhibitors may prolong effects of dopamine; beta-adrenergic blockers may antagonize peripheral vasoconstriction caused by high doses of dopamine; butyrophenones (eg, haloperidol) and phenothiazines can suppress dopaminergic renal and mesenteric vasodilation induced with low-dose dopamine infusion; concurrent administration of diuretic agents with low-dose dopamine may produce additive effects on urine flow; hypotension and bradycardia may occur with phenytoin; dopamine may decrease effects of phenytoin
Documented sensitivity to dopamine-related products; pheochromocytoma; ventricular fibrillation
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Closely monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during the infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia; patients that have received MAO inhibitors within 2-3 wk prior to administration of dopamine, should receive initial doses no greater than 1/10 initial dose; ventricular arrhythmias and hypertension may occur when administering dopamine to patients receiving cyclopropane or halogenated hydrocarbon anesthetics
Norepinephrine (Levophed)
Naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. Stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction. Increases blood pressure and afterload. Increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Generally reserved for use in patients with severe hypotension (eg, systolic blood pressure <70 mm Hg) or hypotension unresponsive to other medication.
Adult
2-12 mcg/min IV infusion; start 0.5-1 mcg/min and titrate upwards; refractory shock may require up to 30 mcg/min; drug should ideally be administered via central venous line
Pediatric
0.1-2 mcg/kg/min IV; start 0.05-0.1 mcg/kg/min; 2 mcg/kg/min maximum dose; should ideally be administered via central venous line
Effects increase when administered concurrently with tricyclic antidepressants, MAO inhibitors, antihistamines, guanethidine, methyldopa, ergot alkaloids; atropine may block reflex tachycardia caused by norepinephrine and enhances pressor response
Documented hypersensitivity; peripheral or mesenteric vascular thrombosis because ischemia may be increased and the area of the infarct extended; hypercapnia, volume depletion, caution if sulfite allergy
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Correct blood-volume depletion, if possible, before giving norepinephrine therapy; extravasation may cause severe tissue necrosis and, thus, should be administered into a large vein; caution in occlusive vascular disease
Antidotes
These agents are used in select cases for patients with third-degree block secondary to digoxin toxicity. They should receive digoxin-specific antidote.
Digoxin immune Fab (Digibind)
Immunoglobulin fragment with a specific and high affinity for both digoxin and digitoxin molecules. Removes digoxin or digitoxin molecules from tissue-binding sites.
Each vial of Digibind contains 40 mg of purified digoxin-specific antibody fragments, which will bind approximately 0.6 mg of digoxin or digitoxin.
The dose of antibody depends on total body load (TBL) of digoxin; estimates of TBL can be made in 3 ways:
(1) Estimate the quantity of digoxin ingested in the acute ingestion and assume 80% bioavailability (x mg ingested X 0.8 = TBL)
(2) Obtain a serum digoxin concentration and, using a pharmacokinetics formula, incorporate the Vd of digoxin and the patient's body weight in kg (TBL = digoxin serum level [ng/mL] X 6 L/kg X body weight in kg)
(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, it may be administered empirically (safest to use the largest calculated estimate); alternatively, be prepared to increase dosing if resolution is incomplete.
Adult
Number of vials = Amount ingested (in mg) X 0.8/0.5
For example, for a patient who ingests 10 mg of digoxin, 16 vials should be administered
For a patient who ingests digitoxin instead of digoxin, substitute "1" for "0.8" in above formula, as digitoxin has higher bioavailability than digoxin
If digoxin concentration is known, the number of vials to administer can be calculated by the following formula:
Number of vials = Concentration (ng/mL) X weight (in kg)/100
For example, for a 100-kg male with digoxin concentration of 10 ng/mL, administer 10 vials of Digibind
If amount ingested is not known, then 10 vials can be empirically administered
Pediatric
Not established
None reported
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiac and renal failure; hypokalemia may occur following reversal of digoxin intoxication
Sympathomimetic agents
These agents act on beta-adrenergic receptors and increase heart rate and contractility.
Isoproterenol (Isuprel)
Synthetic sympathomimetic acting directly on beta-receptors. Should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged. Cardiac ischemia or high cardiac risk profile suggesting possible coronary artery disease is contraindication for use. Telemetry monitoring should always accompany use of this agent because of risks of proarrhythmia.
Adult
0.5-2 mcg/min IV infusion, titrate prn to desired effect (emergent use range 2-10 mcg/min)
Pediatric
0.5 mcg/min IV infusion, titrate prn to desired effect
Bretylium increases action of vasopressors on adrenergic receptors, which may in turn result in arrhythmias; guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; tricyclic antidepressants may potentiate pressor response of direct-acting vasopressors
Documented hypersensitivity; tachyarrhythmias, tachycardia or heart block caused by digitalis intoxication, ventricular arrhythmias which require inotropic therapy, and angina pectoris
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, isoproterenol may have a deleterious effect on the injured or failing heart; in some patients, presumably with organic disease of the AV node and its branches, isoproterenol may paradoxically worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes or hyperthyroidism, and sensitivity to sympathomimetic amines; if heart rate exceeds 110 beats/min, may be advisable to decrease infusion rate or temporarily discontinue infusion
More on Heart Block, Third Degree |
| Overview: Heart Block, Third Degree |
| Differential Diagnoses & Workup: Heart Block, Third Degree |
 Treatment & Medication: Heart Block, Third Degree |
| Follow-up: Heart Block, Third Degree |
| Multimedia: Heart Block, Third Degree |
| References |
| Further Reading |
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References
Narula OS, Scherlag BJ, Javier RP, Hildner FJ, Samet P. Analysis of the A-V conduction defect in complete heart block utilizing His bundle electrograms. Circulation. Mar 1970;41(3):437-48. [Medline].
Rosen KM, Dhingra RC, Loeb HS, Rahimtoola SH. Chronic heart block in adults. Clinical and electrophysiological observations. Arch Intern Med. May 1973;131(5):663-72. [Medline].
Costedoat-Chalumeau N, Georgin-Lavialle S, Amoura Z, Piette JC. Anti-SSA/Ro and anti-SSB/La antibody-mediated congenital heart block. Lupus. 2005;14(9):660-4. [Medline].
Bestetti RB, Cury PM, Theodoropoulos TA, Villafanha D. Trypanosoma cruzi myocardial infection reactivation presenting as complete atrioventricular block in a Chagas' heart transplant recipient. Cardiovasc Pathol. Nov-Dec 2004;13(6):323-6. [Medline].
Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd, Freedman RA, Gettes LS, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. May 27 2008;51(21):e1-62. [Medline].
American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part III. Adult advanced cardiac life support. JAMA. Oct 28 1992;268(16):2199-241. [Medline].
International Laison Committee on Resuscitation. 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Part 4: Advanced life support. Resuscitation. Nov-Dec 2005;67(2-3):213-47. [Medline].
Syverud S. Cardiac pacing. Emerg Med Clin North Am. May 1988;6(2):197-215. [Medline].
Further Reading
Clinical guidelines
Adult basic life support: 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations.Adult basic life support. In: 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation 2005 Nov 29;112(22 Suppl):III5-16.
Advanced life support: 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Advanced life support. In: 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation 2005 Nov 29;112(22 Suppl):III25-54.
Keywords
heart block, third-degree heart block, atrioventricular block, AV block, third-degree atrioventricular block, third-degree AV block, complete heart block, AV node, cardiac conduction system, AV dissociation, atrioventricular dissociation, His bundle
