Approach Considerations
Laboratory studies
A cardiac enzyme evaluation should be ordered for patients with chest pain, patients with risk factors for myocardial infarction, and patients who are otherwise unstable and present with heart failure, hypotension, or pulmonary edema. Young patients with no structural heart defects have a very low risk of myocardial infarction.
Other laboratory tests include the following:
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Electrolyte levels - Should be checked because electrolyte abnormalities can contribute to paroxysmal supraventricular tachycardia (paroxysmal SVT)
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Complete blood count (CBC) - Helps to assess whether anemia is contributing to the tachycardia or ischemia
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Thyroid studies - The results are rarely diagnostic of hyperthyroidism
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Digoxin level - Obtain for patients on digoxin, because paroxysmal SVT is one of the many dysrhythmias that can be caused by supratherapeutic levels of this drug
Electrophysiology
Electrophysiologic studies have dramatically changed the diagnosis of SVT. Intracardiac recordings have helped to map accessory pathways and reentry circuits in patients, and they have also assisted cardiologists and electrophysiologists in understanding the mechanisms behind these tachyarrhythmias.
In a prospective registry, Lauschke et al compared the prevalence of inducible arrhythmias and the clinical outcome in 525 patients with and without ECG documentation. Results showed that a substantial proportion of patients with suspected paroxysmal tachycardia, but without ECG documentation, had inducible supraventricular tachycardias (SVTs) and clinically benefited from an electrophysiological study (EPS). [69]
At present, electrophysiologic studies are generally performed in combination with radiofrequency catheter ablation.
Imaging Studies
Chest radiography
Obtain a chest radiograph to assess for the presence of pulmonary edema and cardiomegaly. In certain cases, infections such as pneumonia are also associated with paroxysmal SVT and can be confirmed with chest radiography. [9, 10, 11, 40, 41]
Transthoracic echocardiography
A transthoracic echocardiogram may be helpful if structural or congenital heart disease is suggested.
Magnetic resonance imaging
Cardiac magnetic resonance imaging (MRI) can be useful, especially if a congenital heart disease is being considered.
Electrocardiography
Electrocardiographic findings permit classification of the tachyarrhythmia, and they may allow a precise diagnosis. P waves may not be visible; when present, they may be normal or abnormal, depending on the mechanism of atrial depolarization. [9, 10, 35]
Electrocardiographic characteristics of the various SVTs are as follows:
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Sinus tachycardia - Heart rate greater than 100 bpm; P waves similar to sinus rhythm
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Inappropriate sinus tachycardia (IST) - Findings similar to sinus tachycardia; P waves similar to sinus rhythm
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Sinus nodal reentrant tachycardia (SNRT) - P waves similar to sinus rhythm; abrupt onset and offset
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Atrial tachycardia - Heart rate 120-250 bpm; P-wave morphology different from sinus rhythm; long RP interval (in general); AV block does not terminate tachycardia
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Multifocal atrial tachycardia - Heart rate 100-200 bpm; 3 or more different P-wave morphologies
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Atrial flutter- Atrial rate of 200-300 bpm; flutter waves; AV conduction of 2:1 or 4:1
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Atrial fibrillation - Irregularly irregular rhythm; lack of discernible P waves
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AV nodal reentrant tachycardia (AVNRT) - Heart rate of 150-200 bpm; P wave located either within the QRS complex or shortly after the QRS complex; short RP interval in typical AVNRT and long RP interval in atypical AVNRT
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AV reentrant tachycardia (AVRT) - Heart rate of 150-250 bpm; narrow QRS complex in orthodromic conduction and wide QRS in antidromic conduction; diagnosis excluded by AV block during SVT; P wave after QRS complex
Following the termination of the tachycardia, an ECG should be performed during the sinus rhythm to screen for WPW syndrome. Holter monitoring also may be useful as it can help to assess the frequency and duration of SVT episodes, although they have a low yield. Echocardiography may be helpful in screening for structural or congenital heart disease.
Characterizing a patient’s SVT by comparing the RP interval to the PR interval is helpful. Long RP tachycardias result when atrial activity precedes the QRS complex. In short RP tachycardias, atrial activity occurs with or shortly after ventricle excitation, and the P wave is found within the QRS complex or shortly after the QRS complex. [9, 10, 40, 41] The classifications of SVTs based on the RP interval are as follows:
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Short RP tachycardias – Typical AVNRT, AVRT, junctional ectopic tachycardia (JET), and nonparoxysmal junctional tachycardia (NPJT)
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Long RP tachycardias – Sinus tachycardia, SNRT, atrial tachycardia, atrial flutter, atypical AVNRT, and a permanent form of junctional reciprocating tachycardia
Two consecutive P waves without an intervening QRS complex may be due to atrial tachycardias, in some cases, AVNRT, but they are unlikely to be due to AVRT. Vagal maneuvers and nodal blocking agents like adenosine work in AVNRT in some cases, but not in atrial tachycardias. Blocking the tachycardia with adenosine or vagal maneuvers may assist in diagnosing the rhythm as well as treating it.
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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.
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Atrial tachycardia. The patient's heart rate is 151 bpm. P waves are upright in lead V1.
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Multifocal atrial tachycardia. Note the different P-wave morphologies and irregularly irregular ventricular response.
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Atrial flutter. The patient's heart rate is approximately 135 bpm with 2:1 conduction. Note the sawtooth pattern formed by the flutter waves.
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Atrial fibrillation. The patient's ventricular rate varies from 130-168 bpm. The rhythm is irregularly irregular. P waves are not discernible.
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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.
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Same patient as in the previous image. The patient is in sinus rhythm following atrioventricular nodal reentrant tachycardia.
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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.
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Wolff-Parkinson-White pattern. Note the short PR interval and slurred upstroke (delta wave) to the QRS complexes.
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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 occurs only in patients with Wolff-Parkinson-White syndrome. Both patterns may display retrograde P waves after the QRS complexes.
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Orthodromic atrioventricular reentrant tachycardia. This patient has Wolff-Parkinson-White syndrome.
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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.
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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.
