Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Atrial Tachycardia Medication

  • Author: Adam S Budzikowski, MD, PhD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Dec 30, 2015
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent recurrences and complications. Consider using antiarrhythmic agents when the arrhythmia is causing symptoms and does not respond to correction or treatment of underlying diseases. A calcium channel blocker or beta-blocker also may be required as well, in combination therapy.

Calcium channel blockers are especially effective in atrial tachycardia with triggered activity as the underlying mechanism. Beta-blockers can reduce the frequency and severity of atrial tachycardia episodes by controlling ventricular response.

Next

Beta Blockers, Intrinsic Sympathomimetic

Class Summary

Beta-blockers are effective for reducing the frequency and severity of episodes via control of the ventricular response during tachycardia and by reduction of frequency in a subgroup of patients for whom tachycardia is sensitive to catecholamine. Beta-blockers that have intrinsic sympathomimetic activity are capable of demonstrating low-level agonist activity at a beta receptor while also acting as an antagonist.

Acebutolol (Sectral)

 

Acebutolol is a selective, hydrophilic beta-blocking drug, as well as a class II antiarrhythmic agent with mild, intrinsic sympathomimetic activity. It has a labeled indication for the management of ventricular arrhythmias. Beta-blocker therapy should be tapered gradually rather than withdrawn abruptly, to avoid acute tachycardia, hypertension, and/or ischemia.

Previous
Next

Beta-Blockers, Beta-1 Selective

Class Summary

Beta-blockers are effective for reducing the frequency and severity of episodes, via control of the ventricular response during tachycardia, and for reducing the frequency of episodes in a subgroup of patients whose tachycardia is sensitive to catecholamine. Beta-1 selective drugs are also known as cardioselective agents, because they act on beta-1 receptors on the myocardium.

Atenolol (Tenormin)

 

Atenolol selectively blocks beta-1 receptors, with little or no effect on beta-2 receptors except at high doses. It has an off-label indication for supraventricular and ventricular arrhythmias. Beta-blocker therapy should be tapered gradually to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.

Esmolol (Brevibloc)

 

Because of its brief duration of action (10-30 minutes), esmolol is an excellent drug for use in patients at risk of experiencing complications from beta blockade. It selectively blocks beta-1 receptors, with little or no effect on beta-2 receptors.

Esmolol is also classified as a class II antiarrhythmic agent. It has a labeled indication for the treatment of supraventricular tachycardia (SVT). Beta-blocker therapy should be tapered gradually, to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.

Metoprolol (Lopressor)

 

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG. Metoprolol has an off-label indication for MAT. Beta-blocker therapy should be tapered gradually, to avoid the acute tachycardia, hypertension, and/or ischemia that may occur with abrupt withdrawal.

Previous
Next

Beta Blockers, Nonselective

Class Summary

Beta-blockers reduce the frequency and severity of episodes via control of ventricular response during tachycardia and by reduction of frequency in a subgroup of patients in whom tachycardia is sensitive to catecholamine. Nonselective agents block beta-1 and beta-2 receptors.

Propranolol (Inderal)

 

Propranolol is a class II antiarrhythmic. It is a nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions. Do not administer an IV dose faster than 1 mg/min.

Previous
Next

Antidysrhythmics, III

Class Summary

Many class III antidysrhythmic agents have been shown to be effective in maintaining sinus rhythm after conversion from atrial tachycardia.

Amiodarone (Cordarone, Pacerone, Nexterone)

 

Amiodarone has antiarrhythmic effects that overlap all 4 Vaughn-Williams antiarrhythmic classes. It may inhibit atrioventricular (AV) conduction and sinus node function. It prolongs action potential and the refractory period in myocardium and inhibits adrenergic stimulation. It blocks sodium channels with high affinity for inactive channels, blocks potassium channels, and weakly blocks calcium channels. In addition, this agent noncompetitively blocks alpha- and beta-adrenergic receptors.

Amiodarone has a labeled indication for the management of life-threatening recurrent ventricular fibrillation and hemodynamically-unstable ventricular tachycardia (VT) refractory to other antiarrhythmic agents. It is very effective in converting atrial fibrillation and flutter to sinus rhythm and in suppressing recurrence of these arrhythmias.

Amiodarone is the only agent proven to reduce the incidence and risk of cardiac sudden death, with or without obstruction to left ventricular outflow. With exception of disorders of prolonged repolarization (eg, long QT syndrome), amiodarone may be the drug of choice for life-threatening ventricular arrhythmias refractory to beta blockade and initial therapy with other agents.

Before administering amiodarone, control the ventricular rate and congestive heart failure (if present) with digoxin or calcium channel blockers. Most clinicians are comfortable with inpatient or outpatient loading with 400 mg orally 3 times a day for 1 week, because of low proarrhythmic effect, followed by weekly reductions with the goal of the lowest dose with the desired therapeutic benefit. During loading, patients must be monitored for bradyarrhythmias. With oral dosing, achieving efficacy may take weeks.

Sotalol (Betapace, Betapace AF, Sorine)

 

This class III antiarrhythmic agent blocks K+ channels, prolongs action potential duration, and lengthens the QT interval. It is a non–cardiac-selective beta-adrenergic blocker. Sotalol is effective in the maintenance of sinus rhythm, even in patients with underlying structural heart disease. Class III effects are seen only at oral doses of 160mg/day or higher.

Dofetilide (Tikosyn)

 

Dofetilide is a class III antiarrhythmic agent. It has been approved by the US Food and Drug Administration (FDA) for maintenance of sinus rhythm after conversion from atrial fibrillation or atrial flutter lasting longer than 1 week.

Dofetilide blocks delayed rectifier current and prolongs action potential duration; indeed, even at higher doses it has no effect on other depolarizing potassium currents. It terminates induced reentrant tachyarrhythmias (atrial fibrillation/flutter and VT) and prevents their reinduction. At clinically prescribed concentrations, it has no effect on sodium channels, which are associated with class I effects. Furthermore, no effect is noted on alpha- or beta-adrenergic receptors.

Dofetilide must be initiated with continuous electrocardiographic (ECG) monitoring and monitoring must be continued for 6 doses of the medication. The dose must be individualized according to creatinine clearance (CrCl) and the corrected QT interval (QTc; use the QT interval if the heart rate is less than 60 bpm). There is no information on the use of this drug for heart rates below 50 bpm.

Ibutilide (Corvert)

 

Ibutilide can terminate some atria tachycardias. Ibutilide works by increasing the action potential duration and, thereby, changing atrial cycle-length variability.

Previous
Next

Antidysrhythmics, Ia

Class Summary

These drugs have been tried in patients with refractory recurrent atrial tachycardia and disabling symptoms in whom beta-blockers or calcium channel blockers were unsuccessful. These drugs prolong the atrial refractoriness and slow the conduction velocity, thereby disrupting the reentrant circuit. They also suppress the atrial premature depolarizations that commonly initiate the tachycardia.

Class Ia drugs, which are proarrhythmic, are effective only approximately 50% of the time. Therefore, the use of these agents is limited. In particular, quinidine has been replaced with more effective and safer antiarrhythmic agents and nonpharmacologic therapies.

Procainamide (Procanbid, Pronestyl)

 

Procainamide increases the refractory period of atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity. Procainamide has a labeled indication for the treatment of life-threatening ventricular arrhythmias. It is indicated in recurrent VT not responsive to lidocaine, refractory SVT, refractory ventricular fibrillation, pulseless VT, and atrial fibrillation with rapid rate in Wolff-Parkinson-White syndrome.

Previous
Next

Antidysrhythmics, Ic

Class Summary

These agents have been used in patients with atrial tachycardia and disabling symptoms in whom beta-blockers or calcium channel blockers were unsuccessful. Recommended use is with a beta-blocker or calcium channel blocker.

Flecainide (Tambocor)

 

Flecainide blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart. This agent increases electrical stimulation of the threshold of the ventricle and His-Purkinje system, and by shortening phase 2 and 3 repolarization, it decreases action potential duration and effective refractory periods.

Flecainide is indicated for the treatment of paroxysmal atrial fibrillation/flutter associated with disabling symptoms and paroxysmal SVTs, including AV nodal reentrant tachycardia, AV reentrant tachycardia, and other SVTs of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. It is also indicated for prevention of documented life-threatening ventricular arrhythmias (eg, sustained VT). It is not recommended in less severe ventricular arrhythmias, even if patients are symptomatic.

Propafenone (Rythmol)

 

Propafenone shortens upstroke velocity (phase 0) of the monophasic action potential. It reduces fast inward current carried by sodium ions in Purkinje fibers and, to a lesser extent, myocardial fibers, and it may increase the diastolic excitability threshold and prolong the effective refractory period. Propafenone reduces spontaneous automaticity and depresses triggered activity.

This agent is indicated for the treatment of documented life-threatening ventricular arrhythmias (eg, sustained VT). Propafenone appears to be effective in the treatment of SVTs, including atrial fibrillation and flutter. It is not recommended in patients with less severe ventricular arrhythmias, even if symptomatic.

Previous
Next

Calcium Channel Blockers

Class Summary

Via specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity. They are especially effective in atrial tachycardia, with triggered activity as the underlying mechanism.

Diltiazem (Cardizem CD, Cardizem SR, Dilacor, Tiazac)

 

During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. Diltiazem injection has a labeled indication for the conversion of paroxysmal SVT and control of rapid ventricular rate in patients with atrial fibrillation and atrial flutter.

Verapamil (Calan, Calan SR, Covera HS, Verelan)

 

During depolarization, verapamil inhibits calcium ions from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium. It has a labeled indication for the treatment of ST.

Previous
Next

Antidysrhythmics, V

Class Summary

Digoxin and adenosine alter the electrophysiologic mechanisms responsible for arrhythmia. Digitalis in toxic doses can cause atrial tachycardia. In therapeutic doses, digitalis may be useful in some focal atrial tachycardias. It should be considered if beta-blockers are contraindicated or if beta-blockers and calcium channel blockers are unsuccessful in controlling the arrhythmia medically.

Adenosine is an ultra–short-acting drug that is useful in diagnosing SVTs of unknown origin, in terminating SVTs that are dependent on the AV junction, and in some focal atrial tachycardias. If adenosine successfully terminates an atrial tachycardia, the patient may respond to beta-blockers or calcium channel blockers.

Magnesium sulfate

 

Magnesium is used for replacement therapy in magnesium deficiency, especially in acute hypomagnesemia accompanied by signs of tetany similar to those observed in hypocalcemia. When magnesium sulfate is administered to correct hypokalemia, most patients convert to normal sinus rhythm. In a small number of patients with normal potassium levels, high-dose magnesium levels cause a significant decrease in the patient's heart rate and conversion to normal sinus rhythm.

Magnesium is the drug of choice for torsade de pointes and also may be useful for treating conventional VT, especially when hypomagnesemia is confirmed. When administering treatment with magnesium sulfate, monitor for hypermagnesemia because overdose can cause cardiorespiratory collapse and paralysis.

Digoxin (Lanoxicaps, Lanoxin)

 

Digoxin is a cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. It acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure. It is used to control the ventricular rate when administering propafenone, flecainide, or procainamide.

To achieve a total digitalizing dose, initially administer 50% of the dose. Then administer the remaining two 25% portions at 6- to 12-hour intervals (ie, 1/2, 1/4, 1/4).

Adenosine (Adenocard, Adenoscan)

 

Adenosine is a short-acting agent that alters potassium conductance into cells and results in hyperpolarization of nodal cells. This increases the threshold to trigger an action potential and results in sinus slowing and blockage of AV conduction. As a result of its short half-life, adenosine is best administered in an antecubital vein as an IV bolus followed by rapid saline infusion.

Adenosine is a first-line medical treatment for termination of paroxysmal SVT. It is effective in terminating AV nodal reentrant tachycardia and AV reciprocating tachycardia. More than 90% of patients convert to sinus rhythm with adenosine 12 mg.

Previous
 
Contributor Information and Disclosures
Author

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

Disclosure: Received consulting fee from Boston Scientific for speaking and teaching; Received honoraria from St. Jude Medical for speaking and teaching; Received honoraria from Zoll for speaking and teaching.

Coauthor(s)

Christine S Cho, MD, MPH, MEd Assistant Professor, Departments of Pediatrics and Emergency Medicine, University of California, San Francisco, School of Medicine

Christine S Cho, MD, MPH, MEd is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

Mirna M Farah, MD Associate Professor of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Division of Emergency Medicine, Children's Hospital of Philadelphia

Mirna M Farah, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Dariusz Michałkiewicz, MD Head, Electrophysiology Department, Military Medical Institute, Poland

Disclosure: Nothing to disclose.

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 A Peak, MD Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary

David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Pfizer Salary Employment

Justin D Pearlman, MD, PhD, ME, MA Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center

Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

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

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

References
  1. Weber R, Letsas KP, Arentz T, Kalusche D. Adenosine sensitive focal atrial tachycardia originating from the non-coronary aortic cusp. Europace. 2009 Jun. 11(6):823-6. [Medline].

  2. Ma G, Brady WJ, Pollack M, Chan TC. Electrocardiographic manifestations: digitalis toxicity. J Emerg Med. 2001 Feb. 20(2):145-52. [Medline].

  3. McCord J, Borzak S. Multifocal atrial tachycardia. Chest. 1998 Jan. 113(1):203-9. [Medline].

  4. Lennox EG. Cardiology. Arcara KM, Tschudy MM, eds. Johns Hopkins: The Harriet Lane Handbook. 19th ed. Philadelphia, PA: Mosby Elsevier Inc; 2012.

  5. Song MK, Baek JS, Kwon BS, Kim GB, Bae EJ, Noh CI, et al. Clinical spectrum and prognostic factors of pediatric ventricular tachycardia. Circ J. 2010 Sep. 74(9):1951-8. [Medline].

  6. Shine KI, Kastor JA, Yurchak PM. Multifocal atrial tachycardia. Clinical and electrocardiographic features in 32 patients. N Engl J Med. 1968 Aug 15. 279(7):344-9. [Medline].

  7. Wu RC, Berger R, Calkins H. Catheter ablation of atrial flutter and macroreentrant atrial tachycardia. Curr Opin Cardiol. 2002 Jan. 17(1):58-64. [Medline].

  8. Knecht S, Veenhuyzen G, O'Neill MD, Wright M, Nault I, Weerasooriya R, et al. Atrial tachycardias encountered in the context of catheter ablation for atrial fibrillation part ii: mapping and ablation. Pacing Clin Electrophysiol. 2009 Apr. 32(4):528-38. [Medline].

  9. Hirai Y, Nakano Y, Yamamoto H, Ogi H, Yamamoto Y, Suenari K, et al. Pulmonary artery mapping for differential diagnosis of left-sided atrial tachycardia. Circ J. 2013. 77(2):345-51. [Medline].

  10. Chen SA, Chiang CE, Yang CJ, et al. Sustained atrial tachycardia in adult patients. Electrophysiological characteristics, pharmacological response, possible mechanisms, and effects of radiofrequency ablation. Circulation. 1994. 90(3):1262-78.

  11. Chung H, Joung B, Lee KY, et al. Left Atrial Volume Index Predicts Recurrence of Stroke in Patients with Nonsustained Atrial Tachycardia. J Stroke Cerebrovasc Dis. 2015 Oct. 24 (10):2408-15. [Medline].

  12. [Guideline] Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol. 2003 Oct 15. 42(8):1493-531. [Medline]. [Full Text].

  13. Tucker KJ, Law J, Rodriques MJ. Treatment of refractory recurrent multifocal atrial tachycardia with atrioventricular junction ablation and permanent pacing. J Invasive Cardiol. 1995 Sep. 7(7):207-12. [Medline].

  14. Kastor JA. Multifocal atrial tachycardia. N Engl J Med. 1990 Jun 14. 322(24):1713-7. [Medline].

  15. Cohen L, Kitzes R, Shnaider H. Multifocal atrial tachycardia responsive to parenteral magnesium. Magnes Res. 1988 Dec. 1(3-4):239-42. [Medline].

  16. Iseri LT, Fairshter RD, Hardemann JL, Brodsky MA. Magnesium and potassium therapy in multifocal atrial tachycardia. Am Heart J. 1985 Oct. 110(4):789-94. [Medline].

  17. McCord JK, Borzak S, Davis T, Gheorghiade M. Usefulness of intravenous magnesium for multifocal atrial tachycardia in patients with chronic obstructive pulmonary disease. Am J Cardiol. 1998 Jan 1. 81(1):91-3. [Medline].

  18. Ho KM. Intravenous magnesium for cardiac arrhythmias: jack of all trades. Magnes Res. 2008 Mar. 21(1):65-8. [Medline].

  19. Parillo JE. Treating Multifocal Atrial Tachycardia (MAT) in a critical care unit: new data regarding verapamil and metoprlol. Update Crit Care Med. 1987. 2:3-5.

  20. Arsura E, Lefkin AS, Scher DL, Solar M, Tessler S. A randomized, double-blind, placebo-controlled study of verapamil and metoprolol in treatment of multifocal atrial tachycardia. Am J Med. 1988 Oct. 85(4):519-24. [Medline].

  21. Arsura EL, Solar M, Lefkin AS, Scher DL, Tessler S. Metoprolol in the treatment of multifocal atrial tachycardia. Crit Care Med. 1987 Jun. 15(6):591-4. [Medline].

  22. Hazard PB, Burnett CR. Treatment of multifocal atrial tachycardia with metoprolol. Crit Care Med. 1987 Jan. 15(1):20-5. [Medline].

  23. Adcock JT, Heiselman DE, Hulisz DT. Continuous infusion diltiazem hydrochloride for treatment of multifocal atrial tachycardia (abstract). Clin Res. 1994. 42:430A.

  24. Aronow WS, Plasencia G, Wong R. Effect of verapamil versus placebo on PAT and MAT. Current Ther Res. 1980. 27:823-29.

  25. Hazard PB, Burnett CR. Verapamil in multifocal atrial tachycardia. Hemodynamic and respiratory changes. Chest. 1987 Jan. 91(1):68-70. [Medline].

  26. Levine JH, Michael JR, Guarnieri T. Treatment of multifocal atrial tachycardia with verapamil. N Engl J Med. 1985 Jan 3. 312(1):21-5. [Medline].

  27. Salerno DM, Anderson B, Sharkey PJ, Iber C. Intravenous verapamil for treatment of multifocal atrial tachycardia with and without calcium pretreatment. Ann Intern Med. 1987 Nov. 107(5):623-8. [Medline].

  28. Kouvaras G, Cokkinos DV, Halal G, Chronopoulos G, Ioannou N. The effective treatment of multifocal atrial tachycardia with amiodarone. Jpn Heart J. 1989 May. 30(3):301-12. [Medline].

  29. Hsieh MY, Lee PC, Hwang B, Meng CC. Multifocal atrial tachycardia in 2 children. J Chin Med Assoc. 2006 Sep. 69(9):439-43. [Medline]. [Full Text].

  30. Kuralay E, Cingöz F, Kiliç S, Bolcal C, Günay C, Demirkiliç U, et al. Supraventricular tachyarrythmia prophylaxis after coronary artery surgery in chronic obstructive pulmonary disease patients (early amiodarone prophylaxis trial). Eur J Cardiothorac Surg. 2004 Feb. 25(2):224-30. [Medline].

  31. Pierce WJ, McGroary K. Multifocal atrial tachycardia and Ibutilide. Am J Geriatr Cardiol. 2001 Jul-Aug. 10(4):193-5. [Medline].

  32. Barranco F, Sanchez M, Rodriguez J, Guerrero M. Efficacy of flecainide in patients with supraventricular arrhythmias and respiratory insufficiency. Intensive Care Med. 1994. 20(1):42-4. [Medline].

 
Previous
Next
 
This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note that the negative P waves in leads III and aVF (upright arrows) are different from the sinus beats (downward arrows). The RP interval exceeds the PR interval during the tachycardia. Note also that the tachycardia persists despite the atrioventricular block.
Propagation map of right atrial tachycardia originating from the right atrial appendage obtained with non-contact mapping using EnSite mapping system.
Note that the atrial activities originate from the right atrium and persist despite the atrioventricular block. These features essentially exclude atrioventricular nodal reentry tachycardia and atrioventricular tachycardia via an accessory pathway. Note also that the change in the P wave axis at the onset of tachycardia makes sinus tachycardia unlikely.
Anterior-posterior projection is shown. An example of activation mapping using contact technique and EnSite system. The atrial anatomy is partially reconstructed. Early activation points are marked with white/red color. The activation waveform spreads from the inferior/lateral aspect of the atrium through the entire chamber. White points indicate successful ablation sites that terminated the tachycardia. TV – Tricuspid valveCS – Shadow of the catheter inserted in the coronary sinus
Intracardiac tracings showing atrial tachycardia breaking with application of radiofrequency energy. Before ablation, the local electrograms from the treatment site preceded the surface P wave by 51 ms, consistent with this site being the source of the tachycardia. Note that postablation electrograms on the ablation catheter are inscribed well past the onset of the sinus rhythm P wave. The first 3 tracings show surface electrocardiograms as labeled.CS – Respective pair of electrodes of the coronary sinus catheterCS 7,8 – Located at the os of the coronary sinusCS 1,2 – Distal pair of electrodes Abl – Ablation catheter (D-distal pair of electrodes)
An example of rapid atrial tachycardia mimicking atrial flutter. A single radiofrequency application terminates the tachycardia. The first 3 tracings show surface electrocardiograms, as labeled. HRA – High right atrial catheter RVA – Catheter located in right ventricular apex HBED and HBEP – Respectively, distal and proximal pair of electrodes in the catheter located at His bundle AblD and AblP – Respectively, distal and proximal pair of electrodes of the mapping catheter MAP – Unipolar electrograms from the tip of the mapping catheter
Electrocardiogram showing multifocal atrial tachycardia (MAT).
This electrocardiogram belongs to an asymptomatic 17-year-old male who was incidentally discovered to have Wolff-Parkinson-White (WPW) pattern. It shows sinus rhythm with evident preexcitation. To locate the accessory pathway (AP), the initial 40 milliseconds of the QRS (delta wave) are evaluated. Note that the delta wave is positive in lead I and aVL, negative in III and aVF, isoelectric in V1, and positive in the rest of the precordial leads. Therefore, this is likely a posteroseptal AP.
This is a 12-lead electrocardiogram from an asymptomatic 7-year-old boy with Wolff-Parkinson-White (WPW) pattern. Delta waves are positive in leads I and aVL; negative in II, III, and aVF; isoelectric in V1; and positive in the rest of the precordial leads. This again predicts a posteroseptal location for the accessory pathway (AP).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.