Atrial Tachycardia Clinical Presentation

  • Author: Adam S Budzikowski, MD, PhD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Mar 29, 2011
 

History

Patients with focal atrial tachycardia usually present with episodic or paroxysmal atrial tachycardia. Typically, atrial tachycardia manifests as a sudden onset of palpitations. If atrial tachycardia is due to enhanced automaticity, it may be nonsustained but repetitive or continuous or sustained, as in reentrant forms of atrial tachycardia.

Patients may present with a tachycardia that gradually speeds up soon after its onset (warm-up phenomenon). However, the patient may be unaware of this. This finding during ECG monitoring, as with a Holter, is suggestive that the supraventricular tachycardia is atrial tachycardia. If the tachycardic episodes are accompanied by palpitations, patients also may report dyspnea, dizziness, light-headedness, fatigue, or chest pressure. One should recognize the early manifestations of tachycardia-induced cardiomyopathy (ie, a decline in effort tolerance and symptoms of heart failure in patients with frequent or incessant tachycardias).

Light-headedness may result from relative hypotension, depending on the heart rate and other factors, such as the state of hydration and particularly the presence of structural heart disease. The faster the heart rate, the more likely a patient is to feel light-headed. If the patient has a rapid rate and severe hypotension, syncope may occur.

Reentrant atrial tachycardia is not uncommon in patients with a history of a surgically repaired atrial septal defect. The scar tissue in the atrium may give rise to the formation of a reentrant circuit.

Underlying disorders in multifocal atrial tachycardia

In patients with multifocal atrial tachycardia (MAT), the history may disclose an underlying illness that is causing the tachycardia. Such illnesses include pulmonary, cardiac, metabolic, and endocrinopathic disorders.

Chronic obstructive pulmonary disease (COPD) is the most common underlying disease process (60%). The arrhythmia is commonly precipitated by exacerbation of COPD, sometimes due to infection or exacerbation of heart failure. Increasing hypoxemia with respiratory acidosis and advanced disease also leads to increased bronchodilator usage, thereby increasing catecholamine levels, which may contribute to development of MAT.

Patients with MAT frequently have structural heart disease, mainly coronary artery disease and valvular heart disease, often in conjunction with COPD. Heart failure is often present when the diagnosis of MAT is first made. Metabolic disorders may also lead to MAT. In various series, 24% of patients with MAT were found to have diabetes mellitus. Fourteen percent had hypokalemia, and 14% had azotemia.

Twenty-eight percent of patients with MAT are recovering from major surgery, while others have postoperative infections, sepsis, pulmonary embolism, and CHF. The link between pulmonary embolism and MAT is weak (ie, 6-14% of such patients have been said to have MAT), but the methods of diagnosing pulmonary embolism have not been well documented. Finally, experimental evidence demonstrates that IV cocaine use may lead to the development of MAT.

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Physical Examination

The primary abnormality noted upon physical examination is a rapid pulse rate. In most atrial tachycardias, this is regular. However, in rapid atrial tachycardias with variable AV conduction and in MAT, the pulse may be irregular.

Blood pressure may be low in patients presenting with fatigue, light-headedness, or presyncope. The cardiovascular examination should be aimed at excluding underlying structural heart diseases such as valvular abnormalities and evidence of heart failure.

Depending upon comorbid conditions or general health status, the patient may be hemodynamically unstable. However, determining whether this is due to the underlying condition or the arrhythmia may be difficult.

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Contributor Information and Disclosures
Author

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

Disclosure: Boston Scientific Consulting fee Consulting; St. Jude Medical Honoraria Speaking and teaching; Zoll Honoraria Speaking and teaching

Coauthor(s)

Paul Blackburn, DO, FACOEP, FACEP  Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

Robin R Hemphill, MD, MPH  Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Edmond A Hooker II, MD, DrPH, FAAEM  Assistant Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine

Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

Michael A Huott, MD  Consulting Staff, Department of Emergency Medicine, Southwest Texas Methodist Hospital

Disclosure: Nothing to disclose.

Pratap C Reddy, MD  Joe E Holoubek Professor of Medicine, Professor of Anesthesiology, Louisiana State University School of Medicine in Shreveport

Pratap C Reddy, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Heart Association, and American Medical Association

Disclosure: Nothing to disclose.

Neeraj Tandon, MBBS  Chief, Cardiology Section, Associate Professor of Medicine, Medical Service, Overton Brooks Veterans Affairs Medical Center

Neeraj Tandon, MBBS is a member of the following medical societies: American College of Cardiology and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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 FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Li Zhou, MD, Grzegorz Rozmus, MD, James P Daubert, MD, David Huang, MD, Andrzej M Okreglicki, MB, ChB, MMed, Hongsheng M Guo, MD, and Dariusz Michałkiewicz, MD, to the development and writing of the source articles.

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Propagation map of right atrial tachycardia originating from the right atrial appendage obtained with non-contact mapping using Ensite mapping system.
This 12-lead electrocardiogram demonstrates an atrial tachycardia at a rate of approximately 150 beats per minute. Note 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.
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 thought 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. The local electrograms in the successful site preceded the surface P wave by 51 ms, consistent with successful site. Note that postablation electrograms on the ablation catheter is inscribed well past the onset of 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. Single radiofrequency application terminates the tachycardia. The first 3 tracings show surface electrocardiograms, as labeled. HRA – High right atrial catheterRVA – Catheter located in right ventricular apexHBED and HBEP – Respectively, distal and proximal pair of electrodes in the catheter located at His bundleAblD and AblP – Respectively, distal and proximal pair of electrodes of the mapping catheterMAP – Unipolar electrograms from the tip of the mapping catheter
ECG showing multifocal atrial tachycardia (MAT).
 
 
 
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