Supraventricular Tachycardia, Initial Diagnosis and Treatment
When supraventricular tachycardia (SVT) causes symptoms, it requires immediate medical attention. Although many physicians believe that the precise type of SVT must be identified before providing treatment, this is not true: treatment can often be started safely and effectively without knowing the exact SVT, by tailoring it to the characteristics of the ventricular response as seen on the electrocardiogram (ECG) and history.
Defining Characteristics of Ventricular Response in Supraventricular Tachycardia
- Tempo of onset of tachycardia (sudden, or gradual)
- Heart rate
- Regular vs. Irregular
These characteristics vary between the 7 types of supraventricular tachycardia (SVT), and atrial premature contractions (not technically an SVT, but included as a common “SVT masquerader”):
|SVT||Onset||Reg?||Rate||P-QRS Relationship||After Adenosine||Causes|
|Sinus Tach||Slow||Reg||220 minus age||P before QRS||Transient slowing||Hypovolemia, sepsis, pain, PE, MI, anxiety, exercise, hyperthyroid, CHF|
|Irreg||100-220||Fibrillatory “squiggle,” no P waves [ECG]||Ventricular rate slows transiently||Heart or lung disease, hyperthyroidism, surgery, PE, sepsis|
|Atrial flutter||Sudden||Reg*||150||Flutter waves usu. 2:1 [ECG]||Ventricular rate slows transiently||Heart disease|
|Multifocal atrial tach||Slow||Irreg||100-150||Ps change appearance before QRS [ECG]||No response||Lung disease (usu. COPD), theophylline|
|AVNRT**||Sudden||Reg||150-250||No Ps; or, small P (R’) after QRS [ECG]||Tachycardia stops||None known|
|AVRT‡ incl. WPW||Sudden||Reg||150-250||P after narrow QRS; when wide QRS or a-fib+WPW, no Ps [ECG]||Tachycardia stops||Usually unknown; Ebstein’s anomaly rarely|
|Atrial premature contractions||Slow||Irreg||100-150||P before QRS [ECG]||No response||Stimulants, incl. caffeine|
|Atrial tach||Sudden||Reg||150-250||P before QRS [ECG], often in bursts||Tachycardia stops in ~70%||Heart and lung disease|
* Atrial flutter may be irregular if variable AV conduction is present.
** AVNRT = Atrioventricular node re-entrant tachycardia.
‡ AVRT = Atrioventricular reciprocating tachycardia; WPW = Wolff-Parkinson White syndrome.
How to Evaluate Supraventricular Tachycardia (SVT)
If a patient does not have a pulse, don’t call it supraventricular tachycardia (SVT): it’s cardiac arrest with pulseless electrical activity (PEA). Start CPR and manage according to ACLS PEA algorithms. For more stable patients, evaluate SVT step-wise as follows.
First, don’t look at the P waves: look at the ventricular response to whatever is going on in the atria. Then ask:
- Is the QRS complex wide or narrow?
- Are the QRS’s regular or irregular? (Regular is < 10% variation beat-to-beat, usually <5% in regular tachycardias).
- Was the onset sudden, or slow (by history, and cardiac monitoring at the time of onset, if any)?
Then look for P waves, keeping in mind these principles and pitfalls:
- P waves follow the QRS in AVRT and AVRT; in all other SVTs, they precede the QRS, if Ps are present.
- In SVTs with rapid ventricular rates, P waves are often obscured by the T waves, but may be seen as a “hump” on the T.
- A heart rate of 150 should make you suspect atrial flutter is present.
Narrow QRS Complex SVT. When tachycardia has a narrow QRS complex, it’s much easier to diagnose it as supraventricular tachycardia. Identify the SVT type using the differential diagnosis in the American College of Cardiology (ACC) narrow QRS complex SVT algorithm.
Wide QRS Complex Tachycardia. The origin of wide QRS tachycardias can be either atrial (if a bundle branch block or accessory pathway is present) or ventricular (V-tach, V-fib), so they are trickier, and often more dangerous. Use the American Heart Association (AHA) algorithm for the differential diagnosis of Wide QRS tachycardias (and call a cardiologist).
How to Manage Supraventricular Tachycardia
The AHA’s management algorithm for tachycardia provides a good overview. Electric cardioversion is advised for all unstable tachycardias with a pulse (i.e., with hypotension, altered mental status, pulmonary edema, profound distress, etc). NEJM author Mark Link argues adenosine can be tried first, as it can convert some unstable patients to stable. Adenosine should not be given to people with “bronchospastic lung disease” — mainly, asthma with a history of significant bronchospasm. Dr. Link also advises against calcium channel blockers for first-line use in the diagnosis/treatment of SVT, because of their propensity to acutely lower blood pressure.
Dr. Link seems to advise vagal maneuvers followed by adenosine 6 mg if necessary for stable narrow-complex SVT, and also for wide-complex tachycardias that are definitely regular. Stable, irregular wide complex tachycardias are usually Wolff-Parkinson-White syndrome or atrial fibrillation with aberrant conduction, and adenosine should not be given it can induce ventricular fibrillation in these patients. Diltiazem and verapamil should not be used here, as they can cause severe, dangerous hypotension. Antiarrhythmics such as procainamide, ibutilide, lidocaine, amiodarone, and sotalol are safer and more useful agents for stable wide QRS complex irregular tachycardias.
In patients with hemodynamic instability, is the tachycardia the cause, or an effect? Atrial fibrillation, for example, can often occur during the stress of septic shock or coronary ischemia; whether the tachycardia is also contributing to the hypotension (thereby making the SVT “unstable” and requiring cardioversion) can often be impossible to sort out with confidence. Dr. Link points out that in patients with atrial fibrillation with rates less than 150 per minute, the arrhythmia is rarely contributory to any hemodynamic instability.
Mark Link, MD. Evaluation and Initial Treatment of Supraventricular Tachycardia. NEJM 2012; 367: 1438-1448.