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Cardiology > Arrhythmias
Atrioventricular Dissociation
Article Last Updated: Aug 9, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Chirag M Sandesara, MD, Fellow, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics
Chirag M Sandesara is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, and American Medical Association
Coauthor(s):
Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine;
Ram C Sharma, MD, MRCP, Assistant Professor of Medicine, Division of Cardiology, Department of Internal Medicine, University of Utah Health Science Center;
Roger Freedman, MD, Director of Arrhythmia Service, Director of Electrophysiology Fellowship, Professor, Department of Internal Medicine, Division of Cardiology, University of Utah School of Medicine
Editors: Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, MidAmerica Heart Institute, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research Center, MidAmerica Heart Institute of Saint Luke's Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Marschall S Runge, MD, PhD, Marion Covington Distinguished Professor of Medicine, Vice Dean for Clinical Affairs, Chairman, Department of Medicine, University of North Carolina at Chapel Hill School of Medicine; Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital; Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital
Author and Editor Disclosure
Synonyms and related keywords:
atrioventricular dissociation, AV dissociation, A-V dissociation, AV block, A-V block, heart block, complete heart block, bradycardia, tachycardia, AV dyssynchrony, ventricular tachycardia, nonparoxysmal junctional tachycardia, junctional tachycardia, escape junctional rhythm, accelerated idioventricular rhythm
Background
Atrioventricular (AV) dissociation is a condition in which the atria and ventricles do not activate in a synchronous fashion but beat independent of each other. AV dissociation usually refers to the situation in which the ventricular rate is the same or faster than the atrial rate. When the atrial rate is faster and the atria and ventricles are beating independently, complete heart block is present; this is distinct from AV dissociation. While complete heart block can be properly considered a form of AV dissociation, it is discussed in detail in Atrioventricular Block and is not considered further in this article. Also, in AV dissociation, no retrograde ventriculoatrial conduction occurs.
When the atrial rate is the same as the ventricular rate but the P wave is not conducting, the rhythm disturbance is known as isorhythmic AV dissociation. When the rates are similar but occasionally the atria conduct to the ventricles, the rhythm is known as interference AV dissociation.
AV dissociation can be a benign phenomenon and can be complete or incomplete. When incomplete, some of the P waves conduct and capture the ventricles (ie, interference AV dissociation), but if they do not, it is complete AV dissociation. Complete AV dissociation can mimic AV block, but the fact that none of the P waves conduct has more to do with timing of the P waves in relation to the QRS complex rather than the presence of AV block.
Pathophysiology
A normal cardiac impulse arises from the sinus node and is conducted through the AV junction, the bundle of His, and the bundle branches to the ventricles. The sinus node is the dominant pacemaker because its intrinsic rate is faster than subsidiary pacemakers in the AV junction or in the ventricle. AV dissociation can result from (1) slowing of the dominant pacemaker (sinus node), which allows an escape junctional or ventricular rhythm, or (2) acceleration of a normally slower (subsidiary) pacemaker, such as a junctional site or a ventricular site that activates the ventricles without retrograde atrial capture.
Conditions that can initiate AV dissociation include surgical and anesthesia interventions (including intubation), conditions that increase catecholamine levels (including infusions of inotropes) and drugs that block catecholamines, sinus node disease, digoxin toxicity, myocardial infarction and other structural heart disease, hyperkalemia, vagal activation (eg, neurocardiogenic syncope, vomiting), ventricular tachycardia, or ventricular pacing. AV dissociation can be seen after radiofrequency ablation of the slow pathway responsible for AV nodal reentry if some of the vagal fibers are damaged. After exertion, if AV dissociation is present from an escape pacer, it can be a normal phenomenon. Whatever the cause, AV dissociation usually is secondary to some other cause.
Frequency
International
Little epidemiologic information is available regarding the frequency of AV dissociation.
Mortality/Morbidity
AV dissociation by itself can be benign. Any adverse effects are related to ensuing bradycardia, AV dyssynchrony, or underlying conditions.
History
AV dissociation can be asymptomatic, but if symptoms related to AV dissociation are present, they are related to bradycardia, tachycardia, AV dyssynchrony, or loss of atrial "kick" and include the following:
- Exertional dyspnea
- Light-headedness
- Throbbing sensation in neck
- Palpitations
- Fatigue, malaise
Physical
Physical findings are related to bradycardia, tachycardia, AV dyssynchrony, and lack of an atrial kick at least intermittently.
- General appearance - Variable pulse or blood pressure due to the changing relationship between atrial and ventricular contractions
- Pulse - Pulse volume is variable, with fast or slow rates depending on the underlying cause
- Blood pressure - Low in ventricular tachycardia
- Jugular venous pulse - Intermittent cannon a waves are noted when atria and ventricles contract simultaneously; a waves vary as PR interval varies or if the P wave is immediately followed by a QRS
- Heart sounds
- Variable intensity of first heart sound
- Cyclic increase in intensity of first heart sound as PR interval shortens, climaxed by a very loud sound (bruit de cannon); occurs when ventricular rate exceeds atrial rate and QRS occurs just after P wave
- Beat-to-beat variation in systolic murmurs
Causes
Major causes of AV dissociation include ventricular tachycardia, nonparoxysmal junctional tachycardia, escape junctional rhythm, and accelerated idioventricular rhythm.
- Ventricular tachycardia
- Nonparoxysmal junctional tachycardia
- Junctional rhythm/tachycardia occur at a rate faster than the sinus rate, without retrograde atrial capture.
- This is observed in clinical situations such as digoxin toxicity; sinus bradycardia with escape junctional rhythm; and after cardiac surgery, particularly valve surgery or replacement.
- Long postectopic cycle allowing escape junctional rhythm
Atrioventricular Block
Lab Studies
Other Tests
- The electrocardiogram is the most commonly used modality to diagnose this problem. Findings show the underlying rhythm and P-wave morphology. In complete AV dissociation, P waves and QRS complexes have no fixed temporal relationship to each other. P-wave morphology depends on atrial activation.
- The relationship between the atrial and ventricular rates is very important to understanding AV dissociation (see Images 1-2). The ventricular rate is the same or faster than the atrial rate.
- Occasionally, other methods are required to assess atrial and ventricular activation, and the diagnostic approach to AV dissociation is given in Image 3.
- Determining whether a P wave conducts can be difficult. To distinguish AV conduction from AV block, having the patient perform a maneuver to change the atrial and ventricular rate may help. While attached to a monitor, the patient can sit up or can perform some form of exercise.
Medical Care
Treatment depends on the underlying condition and its severity. The important considerations and steps in the treatment of patients with AV dissociation include the hemodynamic status of the patient and recognition of the underlying pathology.
- For patients who are hemodynamically unstable, i.e., patients with ventricular tachycardia, the initial treatment of choice is direct-current cardioversion or intravenous drug therapy, depending on the stability of the patient. Treatment of digoxin toxicity should also be pursued.
- Ascertaining if AV conduction is intact is important in patients with AV dissociation due to an accelerated junctional rhythm following cardiac surgery. Rarely, patients have complete AV block with an accelerated focus distal to the level of block; when the accelerated focus becomes quiescent, heart block is present.
Surgical Care
A permanent pacemaker is rarely necessary.
Consultations
Patients with unexplained or uncorrected persistent symptomatic AV dissociation due to an escape rhythm or ventricular tachycardia may require referral to an electrophysiologist or a cardiologist.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Drug Category: Anticholinergic agents
Competitive inhibitor at autonomic, postganglionic, and cholinergic receptors.
| Drug Name | Atropine Sulfate |
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| Description | Increases heart rate through vagolytic effects, causing increase in cardiac output. |
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| Adult Dose | 0.5-1.0 mg IV or ET q3-5min; not to exceed 3 mg total (0.04 mg/kg) |
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| Pediatric Dose | 0.02 mg/kg/dose IV; minimum of 0.1 mg |
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| Contraindications | Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia |
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| Interactions | Other anticholinergics have additive effects; may increase pharmacologic effects of atenolol and digoxin; may decrease antipsychotic effects of phenothiazines; tricyclic antidepressants with anticholinergic activity may increase effects |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Avoid in Down syndrome and/or children with brain damage to prevent hyperreactive response; avoid in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in patients with prostatic hypertrophy, prostatism is associated with dysuria and may require catheterization |
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Drug Category: Adrenergic agonist agents
Stimulate myocardial performance and improve coronary artery blood flow.
| Drug Name | Isoproterenol (Isuprel, Isopro) |
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| Description | Has beta1- and beta2-adrenergic receptor activity. Binds beta-receptors of heart, smooth muscle of bronchi, skeletal muscle, vasculature, and alimentary tract. Has positive inotropic and chronotropic actions. |
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| Adult Dose | Dilute 1 mL of 1:5000 solution (0.2 mg) with 10 mL saline solution or D5W for injection
Dose: 2-6 mcg/min IV (1-3 mL of diluted solution)
Alternatively, dilute 10 mL of 1:5000 solution (2 mg) in 500 mL of D5W or dilute 5 mL of 1:5000 solution (1 mg) in 250 mL of D5W and administer 5 mcg/min (1.25 mL/min of diluted solution) to achieve heart rate of 90-100 bpm |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; tachyarrhythmias, tachycardia, or heart block caused by digitalis intoxication; ventricular arrhythmias that require inotropic therapy; angina pectoris |
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| Interactions | Tricyclic antidepressants may potentiate pressor response of direct-acting vasopressors |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | May have a deleterious effect on ischemic or failing heart by increasing myocardial oxygen requirements while decreasing effective coronary perfusion; in some patients, presumably with organic disease of AV node and its branches, may paradoxically worsen heart block or precipitate Adams-Stokes attacks; caution in coronary disease, coronary insufficiency, diabetes, hyperthyroidism, and sensitivity to sympathomimetic amines; if heart rate exceeds 110 bpm, may be advisable to decrease infusion rate or temporarily discontinue infusion |
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Drug Category: Antidotes
Used to treat digitalis intoxication.
| Drug Name | Digoxin immune Fab (Digibind) |
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| Description | 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 that 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 calculated in 3 ways, (1) estimate of the quantity of digoxin ingested in the acute ingestion and assume 80% bioavailability (mg ingested X 0.8 = TBL); (2) obtain a serum digoxin concentration and, using a pharmacokinetics formula, incorporate the volume of distribution (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); and (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, administer empirically (safest to use the largest calculated estimate); alternatively, be prepared to increase dosing if resolution is incomplete. Please see PDR for more complete information. |
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| Adult Dose | Suggested: 10 and 5 vials IV for acute and chronic toxicity, respectively |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity |
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| Interactions | None reported |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Caution in cardiac and renal failure; hypokalemia may occur following reversal of digoxin intoxication |
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Deterrence/Prevention
- Close monitoring for medications that can cause AV dissociation
- Correction of electrolyte imbalances
Prognosis
- Depends on the underlying cardiac condition and effects of drug toxicities
Medical/Legal Pitfalls
- Failure to ensure that AV conduction is intact, particularly in patients with accelerated junctional rhythm following cardiac surgery
- Failure to diagnose and correct digoxin toxicity if present
| Media file 1:
Atrioventricular (AV) dissociation. Ventricular tachycardia and complete AV dissociation. P waves are marked. |
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Media type: ECG
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| Media file 2:
Atrioventricular (AV) dissociation. Complete AV block and no fixed relationship between P waves and QRS complexes. |
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Media type: ECG
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| Media file 3:
Diagnostic algorithm for atrioventricular dissociation. |
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Media type: Image
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- Braunwald E. Atrioventricular dissociation. In: Braunwald E, Zipes DP, Libby P, eds. Heart Diseases: A Textbook Of Cardiovascular Medicine. 6th ed. Philadelphia, Pa: WB Saunders Co;. 2001.
- Duffield JS, Jacob AJ, Miller HC. Recurrent, life-threatening atrioventricular dissociation associated with toxoplasma myocarditis. Heart. Nov 1996;76(5):453-4. [Medline].
- Luzza F, Oreto G. Pseudo-atrioventricular dissociation caused by interpolated ventricular extrasystoles in the presence of dual atrioventricular nodal pathway. Chest. May 1994;105(5):1587-9. [Medline].
- Oreto G, Smeets JL, Rodriguez LM, et al. Wide complex tachycardia with atrioventricular dissociation and QRS morphology identical to that of sinus rhythm: a manifestation of bundle branch reentry. Heart. Dec 1996;76(6):541-7. [Medline].
- Pick A. A-V dissociation. A proposal for a comprehensive classification and consistent terminology. Am Heart J. Aug 1963;66:147-50. [Medline].
- Wagner GS. Atrioventricular dissociation. In: Wagner GSS, Marriott HJ, eds. Marriott's Practical Electrocardiography. 9th ed. Baltimore, Md: Williams & Wilkins;. 1994.
Atrioventricular Dissociation excerpt Article Last Updated: Aug 9, 2006
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