AUTHOR INFORMATION

Section 1 of 12

Authored by Michael D Levine, MD, Staff Physician, Department of Emergency Medicine, Brigham and Women's Hospital, Massachusetts General Hospital

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

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

Edited by Theodore Gaeta, DO, MPH, Residency Director, Clinical Associate Professor of Emergency Medicine in Medicine, Department of Emergency Medicine, New York Methodist Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School

Author's Email:	Michael D Levine, MD
Editor's Email:	Theodore Gaeta, DO, MPH

eMedicine Journal, September 5 2006, VOLUME 7, Number 9

INTRODUCTION

Section 2 of 12

Background: Complete heart block, also referred to as third-degree heart block, or third-degree atrioventricular (AV) block, is a disorder of the cardiac conduction system, where there is no conduction through the AV node. Therefore, complete disassociation of the atrial and ventricular activity exists. The ventricular escape mechanism can occur anywhere from the AV node to the bundle-branch Purkinje system. It is important to realize, however, that not all patients with AV dissociation have complete heart block. For example, patients with accelerated junctional rhythms have AV dissociation, but not complete heart block, if the escape rate is faster than the intrinsic sinus rate. Electrocardiographically, complete heart block is represented by QRS complexes being conducted at their own rate and totally independent of the P waves.

Pathophysiology: Complete heart block is caused by a conduction block at the level of the AV node, the bundle of His, or the bundle-branch Purkinje system. In most cases (approximately 61%), the block occurs below the His bundle. Block within the AV node accounts for approximately one fifth of all cases, while block within the His bundle accounts for slightly less than one fifth of all cases.

Duration of the escape QRS complex depends on the site of the block and the site of the escape rhythm pacemaker.

Pacemakers above the His bundle produce a narrow QRS complex escape rhythm, while those at or below the His bundle produce a wide QRS complex.

When the block is at the level of the AV node, the escape rhythm generally arises from a junctional pacemaker with a rate of 45-60 beats per minute. Patients with a junctional pacemaker frequently are hemodynamically stable and their heart rate increases in response to exercise and atropine.

When the block is below the AV node, the escape rhythm arises from the His bundle or the bundle-branch Purkinje system at rates less than 45 beats per minute. These patients generally are hemodynamically unstable and their heart rate is unresponsive to exercise and atropine.

Mortality/Morbidity: Patients with complete heart block are frequently hemodynamically unstable, and as a result, the patient may experience syncope, cardiovascular collapse, or death.

CLINICAL

Section 3 of 12

History: Complete heart block has a wide range of clinical presentations; most patients are symptomatic.

• Patients occasionally are asymptomatic or have only minimal symptoms related to hypoperfusion. In these situations, symptoms include the following:

• Fatigue

• Dizziness

• Impaired exercise tolerance

• Chest pain

• Patients with narrow complex escape rhythms (eg, those whose escape rhythm occurs above the His bundle) are more likely to have minimal symptoms. More commonly, however, the patients are profoundly symptomatic, especially if a wide-complex escape rhythm is present, indicating the origin of the pacemaker is below the His bundle. In such cases, symptoms can include the following:

• Syncope

• Confusion

• Dyspnea

• Severe chest pain

• Sudden death

• Because an acute myocardial infarction is one cause of complete heart block, patients who concurrently experience an MI can have associated symptoms from the MI, including chest pain, dyspnea, nausea or vomiting, and diaphoresis.

• Patients who have a history of cardiac disease may be on medications that affect the conduction system through the AV node, including the following:

• Beta-blockers

• Calcium channel blockers

• Digitalis cardioglycosides

Physical:

• The physical examination will be notable for bradycardia, which can be quite severe.

• Signs of congestive heart failure as a result of decreased cardiac output may be present and include the following:

• Tachypnea or respiratory distress

• Rales

• Jugular venous distention

• Patients may have signs of hypoperfusion, including the following:

• Altered mental status

• Hypotension

• Lethargy

• In patients with concomitant myocardial ischemia or infarction, corresponding signs may be evident on examination:

• Signs of anxiety such as agitation or unease

• Diaphoresis

• Pale or pasty complexion

• Tachypnea

• Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis toxicity. This rhythm occurs because of the junctional escape rhythm.

Causes: Complete heart block can be either congenital or acquired.

• The congenital form usually occurs at the level of the AV node, and patients are relatively asymptomatic at rest but later develop symptoms because the fixed heart rate is not able to adjust for exertion. In the absence of major structural abnormalities, congenital heart block is often associated with maternal antibodies to SS-A (Ro) and SS-B (La).

• Causes of acquired complete heart block include the following:

• Complete heart block can develop from isolated, single-agent overdose, or often from combined or iatrogenic coadministration of AV-nodal, beta-adrenergic, and calcium channel blocking agents. Drugs or toxins associated with heart block include the following:
  • Class Ia antiarrhythmics (eg, quinidine, procainamide, disopyramide)

  • Class Ic antiarrhythmics (eg, flecainide, encainide, propafenone)

  • Class II antiarrhythmics (beta-blockers)

  • Class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide, ibutilide)

  • Class IV antiarrhythmics (calcium channel blockers)

  • Digoxin or other cardiac glycosides

• Infectious causes include the following:
  • Profound hypervagotonicity

  • MI - Anterior wall MI can be associated with an infranodal AV block. Complete heart block develops in slightly less than 10% of cases of acute inferior MI and often resolves within hours to a few days.

  • Cardiomyopathy, eg, Lyme carditis and acute rheumatic fever

  • Metabolic disturbances, eg, severe hyperkalemia

DIFFERENTIALS

Section 4 of 12

Heart Block, Second Degree
Myocardial Infarction
Myocarditis
Sinus Bradycardia

Other Problems to be Considered:

Bradycardia with a ventricular escape
Bradycardia with a junctional escape
Accelerated junctional escape rhythm

WORKUP

Section 5 of 12

Lab Studies:

• Serum electrolytes levels, including potassium and magnesium, to look for metabolic imbalance, indications of renal insufficiency or failure, and particularly for severe hyperkalemia.

• A digoxin level should be obtained for patients on digoxin or in whom ingestion of digoxinlike compounds (eg, Lily of the Valley, Oleander, Foxgrove, Bufonidae toads) is suspected.

• Lyme titers should be obtained from patients who might have been exposed to Lyme disease. Remember that cardiac manifestations of Lyme disease are delayed, so Lyme-induced heart block can occur during any season.

• Myocarditis-related laboratory studies should be performed in patients suspected of having myocarditis. Such studies include Lyme titers, HIV serologies, enterovirus polymerase chain reaction (PCR), adenovirus PCR, and Chagas titers, as clinically appropriate.

• For most patients with illness serious enough to cause third-degree AV block, a complete blood count is indicated to screen for coincident problems (eg, anemia, infection) that may require ED intervention.

Imaging Studies:

• A chest radiograph should be obtained.

• If myocarditis or a pericardial effusion is a concern, an echocardiogram should be performed.

Other Tests:

• Cardiac enzymes are indicated for any patient with suspected myocardial ischemia.

• All patients must have at least one 12-lead electrocardiogram. Ideally, serial electrocardiograms should be performed.

Procedures:

• Cardiac pacing may be initially indicated or may be indicated if a patient deteriorates. Because the situation may be urgent, all patients should have transcutaneous pacing pads applied.

• For patients who are symptomatic (dyspnea, chest pain, myocardial ischemia or MI, CHF, altered mental status), the transcutaneous pacer should be activated immediately. If the external pacer fails to capture, a transvenous pacer should be inserted emergently.

• For patients who are asymptomatic, the transcutaneous pacer should be tested. If the external pacer fails to capture, urgent placement of a transvenous pacer should be considered. Indications for placement would include bradycardia that is ineligible or unresponsive to treatment with medications.

TREATMENT

Section 6 of 12

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, patients in whom capture cannot be obtained with a transcutaneous pacemaker need urgent placement of a transvenous pacemaker, even if the patient is asymptomatic.

• 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.

• Hemodynamically unstable patients for whom timely cardiologic consultation is unavailable should undergo temporary transvenous pacemaker insertion in the ED by the ED physician.

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

Section 7 of 12

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 deinnervated 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.

Drug Category: Anticholinergic agents -- These agents improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade.

Drug Name	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 Dose	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 Dose	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
Contraindications	Documented hypersensitivity to atropine or belladonna alkaloids or related products; concomitant acute myocardial infarction/ischemia; thyrotoxicosis; narrow-angle glaucoma; congestive heart failure; tachycardia
Interactions	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
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Category: 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.

Drug Name	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 Dose	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 Dose	Administer as in adults
Contraindications	Documented sensitivity to dopamine-related products; pheochromocytoma; ventricular fibrillation
Interactions	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
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Name	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 Dose	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 Dose	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
Contraindications	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
Interactions	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
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Category: Antidotes -- These agents are used in select cases for patients with third-degree block secondary to digoxin toxicity. They should receive digoxin-specific antidote.

Drug Name	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 Dose	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 Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in cardiac and renal failure; hypokalemia may occur following reversal of digoxin intoxication

Drug Category: Sympathomimetic agents -- These agents act on beta-adrenergic receptors and increase heart rate and contractility.

Drug Name	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 Dose	0.5-2 mcg/min IV infusion, titrate prn to desired effect (emergent use range 2-10 mcg/min)
Pediatric Dose	0.5 mcg/min IV infusion, titrate prn to desired effect
Contraindications	Documented hypersensitivity; tachyarrhythmias, tachycardia or heart block caused by digitalis intoxication, ventricular arrhythmias which require inotropic therapy, and angina pectoris
Interactions	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
Pregnancy	C - Safety for use during pregnancy has not been established.
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

FOLLOW-UP

Section 8 of 12

Further Inpatient Care:

• The admitting cardiologist will determine the need for and timing of permanent pacemaker implantation.

• All patients with third-degree heart block need to be admitted to either a telemetry floor (if hemodynamically stable and transcutaneous pacing achieves capture) or an intensive care unit. The decision on telemetry versus intensive care should be made in conjunction with the cardiologist.

• Any patient who is hemodynamically unstable, has persistent complete heart block, has electrolyte abnormalities, or who is in complete heart block as a result of an overdose or myocardial infarction should be admitted to the intensive care unit.

Transfer:

• Patients may be transferred to a higher level of care if the hospital does not have intensive care capabilities or if appropriate consultation services (eg, cardiology) are not available.

Deterrence/Prevention:

• Patients with renal insufficiency or failure, dehydration, and certain electrolyte disturbances are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy.

• Patients on multiple nodal agents (eg, beta-blockers and calcium channel blockers) are at an increased risk to develop complete heart block; the more nodal blockade that occurs, the higher the chance of developing complete heart block.

Complications:

• Complications from complete heart block include cardiovascular collapse and death.

• Ventricular arrhythmias from atropine or catecholamines may occur.

• Common complications include those related to line and/or transvenous pacemaker placement. These complications include arterial injury, hemothorax, pneumothorax, or cardiac tamponade.

Patient Education:

• Patients should be educated about possible drug interactions when starting any new medication.

• Patients who are on digoxin should be educated about possible early symptoms of digoxin toxicity.

MISCELLANEOUS

Section 9 of 12

Medical/Legal Pitfalls:

• Failure to initiate temporary transcutaneous or transvenous pacing in a timely fashion

• Failure to interpret cardiac dysrhythmia correctly

• Failure to diagnose and treat underlying etiology of the third-degree block

• Failure to ensure the patient is admitted to an appropriate level of care

• Failure to seek, identify, or treat reversible causes of third-degree AV block, such as hyperkalemia or digoxin toxicity

TEST QUESTIONS

Section 10 of 12

CME Question 1: A 43-year-old man is brought to the ED with ECG evidence of an acute anterior myocardial infarction (MI) complicated by complete heart block. Which of the following is false?

A: The escape rhythm is likely to be wide complex with a rate of 20-45 beats per minute.
B: He may have presented with a Stokes-Adams attack.
C: He is likely to be hemodynamically unstable.
D: The initial treatment of choice for the heart block is atropine.
E: Cardiac consultation is required.

The correct answer is D: Atropine should be withheld in patients with acute MI, as the resulting vagolysis leads to unopposed sympathetic stimulation, causing increased ventricular irritability and, potentially, ventricular tachycardia or ventricular fibrillation. In addition, atropine is ineffective for third-degree block with a wide complex escape rhythm, regardless of cause.

CME Question 2: Which of the following statements is true for patients with complete heart block?

A: Complete heart block in the setting of chronic atrial fibrillation frequently is caused by digitalis toxicity.
B: All patients with complete heart block should undergo urgent placement of a temporary pacing wire.
C: Complete heart block may be caused by anterior myocardial infarction but not by inferior myocardial infarction.
D: Lidocaine or another antiarrhythmic agent should be used to treat a wide complex escape rhythm.
E: Only hemodynamically unstable patients with complete heart block require cardiac consultation and admission.

The correct answer is A: Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis toxicity. The rhythm is regularized because of the junctional escape rhythm.

Pearl Question 1 (T/F): The congenital form of complete heart block is often related to circulating maternal antibodies.

The correct answer is True: Circulating maternal antibodies, often to SS-A (Ro) and SS-B (La), have been associated with the congenital form of complete heart block.

Pearl Question 2 (T/F): An acute anterior myocardial infarction (MI) is the most common cause of infranodal complete heart block.

The correct answer is True: The resulting infranodal complete heart block may require emergency pacing.

Pearl Question 3 (T/F): Cardiac tamponade is a potential complication of placement of a cardiac pacing wire.

The correct answer is True: Hemothorax, pneumothorax, and cardiac tamponade are the main complications.

Pearl Question 4 (T/F): Ventricular tachycardia can cause atrioventricular (AV) dissociation but not complete heart block.

The correct answer is True: Ventricular tachycardia, paroxysmal junctional tachycardia (faster than the native sinus rate), and severe sinus bradycardia with a junctional or ventricular escape mechanism are some conditions that cause AV dissociation but not complete heart block.

PICTURES

Section 11 of 12

Caption: Picture 1. This electrocardiogram demonstrates a patient in complete heart block.
	View Full Size Image
	eMedicine Zoom View (Interactive!)
Picture Type: ECG

BIBLIOGRAPHY

Section 12 of 12

• 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 1992 Oct 28; 268(16): 2199-241[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 2004 Nov-Dec; 13(6): 323-6[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].
• Denes P: Atrioventricular and intraventricular block. Circulation 1987 Apr; 75(4 Pt 2): III19-25[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 2005 Nov-Dec; 67(2-3): 213-47[Medline].
• Rowland E, Morgado F: Sino-atrial node dysfunction, atrioventricular block and intraventricular conduction disturbances. Eur Heart J 1992 Dec; 13 Suppl H: 130-5[Medline].
• Syverud S: Cardiac pacing. Emerg Med Clin North Am 1988 May; 6(2): 197-215[Medline].
• Trigano JA, Birkui PJ, Mugica J: Noninvasive transcutaneous cardiac pacing: modern instrumentation and new perspectives. Pacing Clin Electrophysiol 1992 Nov; 15(11 Pt 2): 1937-43[Medline].

eMedicine Journals > Emergency Medicine > Cardiovascular > Heart Block, Third Degree

Please email us with any comments you have on our new chapter format.

Author Information | Introduction | Clinical | Differentials | Workup | Treatment | Medication | Follow-up | Miscellaneous | Test Questions | Pictures | Bibliography