Paroxysmal Supraventricular Tachycardia Clinical Presentation

  • Author: Monika Gugneja, MD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Jan 23, 2012
 

History

  • Because symptom severity depends on the presence of structural heart disease and on the hemodynamic reserve of the patient, individuals with paroxysmal supraventricular tachycardia may present with mild symptoms or severe cardiopulmonary complaints. Some common presenting symptoms are listed below.[44, 42] Palpitations and dizziness are the most common symptoms reported by patients with SVT. Chest discomfort may be secondary to a rapid heart rate, and it frequently subsides with the termination of the tachycardia. Persistent SVT may lead to tachycardia-induced cardiomyopathy.
  • Common presenting symptoms of paroxysmal supraventricular tachycardia and their frequency rates are as follows:
    • Palpitation - Greater than 96%
    • Dizziness - 75%
    • Shortness of breath - 47%
    • Syncope - 20%
    • Chest pain - 35%
    • Fatigue - 23%
    • Diaphoresis - 17%
    • Nausea - 13%
  • History should include time of onset, any triggers, any previous episodes or arrhythmia, and previous treatment. A detailed past medical and cardiac history and a complete list of all medications should be obtained.
  • Patients who are hemodynamically unstable should be resuscitated immediately with cardioversion. An ECG should be performed as soon as possible.
  • Many patients with frequent episodes of paroxysmal supraventricular tachycardia tend to avoid activities such as exercising and driving due to past episodes of syncope or near-syncope.
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Physical

  • Pertinent findings are generally limited to cardiovascular and respiratory systems. Patients often appear quite distressed. Tachycardia may be the only finding in patients who are otherwise healthy and have significant hemodynamic reserve.
  • Patients who have limited hemodynamic reserve may be tachypneic and hypotensive. Crackles may be auscultated secondary to heart failure. An S3 may be present, and large jugular venous pulsations may also be visualized.[23, 44, 11]
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Causes

Supraventricular tachycardia or paroxysmal supraventricular tachycardia are triggered by reentry mechanism. This may be induced by premature atrial or ventricular ectopic beats. Other triggers include hyperthyroidism and stimulants, including caffeine, drugs, and alcohol.

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Contributor Information and Disclosures
Author

Monika Gugneja, MD  Consulting Staff, Department of Emergency Medicine, William Beaumont Hospital

Disclosure: Nothing to disclose.

Coauthor(s)

Phillip L Kraft, MD  Director, Interventional Cardiology and Cardiac Catheterization Laboratory, William Beaumont Hospital

Phillip L Kraft, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Alan D Forker, MD  Professor of Medicine, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research, MidAmerica Heart Institute of St Luke's Hospital

Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Hypertension, and Phi Beta Kappa

Disclosure: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with no personal profit; Speakers Bureau Honoraria Speaking and teaching

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

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

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.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author James V Talano, MD to the development and writing of this article.

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Sinus tachycardia. Note that the QRS complexes are narrow and regular. The patient's heart rate is approximately 135 bpm. P waves are normal in morphology.
Atrial tachycardia. The patient's heart rate is 151 bpm. P waves are upright in lead V1.
Multifocal atrial tachycardia. Note the different P-wave morphologies and irregularly irregular ventricular response.
Atrial flutter. The patient's heart rate is approximately 135 bpm with 2:1 conduction. Note the sawtooth pattern formed by the flutter waves.
Atrial fibrillation. The patient's ventricular rate varies from 130-168 bpm. Rhythm is irregularly irregular. P waves are not discernible.
Atrioventricular nodal reentrant tachycardia. The patient's heart rate is approximately 146 bpm with a normal axis. Note the pseudo S waves in leads II, III, and aVF. Also note the pseudo R' waves in V1 and aVR. These deflections represent retrograde atrial activation.
Same patient as in Media file 6. Patient is in sinus rhythm following atrioventricular nodal reentrant tachycardia.
Image A displays the slow pathway and the fast pathway, with a regular impulse being conducted through the atrioventricular node. Image B displays a premature impulse that is conducted in an anterograde manner through the slow pathway and in a retrograde manner through the fast pathway, as is seen in typical atrioventricular nodal tachycardia. Image C displays the premature impulse conducting in a retrograde manner through the pathway and the impulse reentering the pathway with anterograde conduction, which is seen commonly in patients with atypical atrioventricular nodal tachycardia.
Wolff-Parkinson-White pattern. Note the short PR interval and slurred upstroke (delta wave) to the QRS complexes.
The left image displays the atrioventricular node with the accessory pathway. The impulse is conducted in an anterograde manner in the atrioventricular node and in a retrograde manner in the accessory pathway. This circuit is known as orthodromic atrioventricular reentrant tachycardia and can occur in patients with concealed accessory tracts or Wolff-Parkinson-White syndrome. The right image displays the impulse being conducted in an anterograde manner through the accessory pathway and in a retrograde manner via the atrioventricular node. This type of circuit is known as antidromic atrioventricular reentrant tachycardia and only occurs in patients with Wolff-Parkinson-White syndrome. Both patterns may display retrograde P waves after the QRS complexes.
Orthodromic atrioventricular reentrant tachycardia. This patient has Wolff-Parkinson-White syndrome.
The left panel depicts antidromic atrioventricular reentrant tachycardia. The right panel depicts sinus rhythm in a patient with antidromic atrioventricular reentrant tachycardia. Note that the QRS complex is an exaggeration of the delta wave during sinus rhythm.
Atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Note the extremely rapid ventricular rate and variability in QRS morphology. Several minutes later, the patient developed ventricular fibrillation.
 
 
 
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