# Tachydysrhythmias: SVT, Atrial Fibrillation, and Wide-Complex Tachycardia

## General Approach to Tachycardia

### Initial Assessment

The first step in evaluating any tachycardia is determining hemodynamic stability. Unstable features include hypotension, altered mental status, acute heart failure, and active ischemia. Any unstable tachycardia with a pulse should receive synchronized cardioversion regardless of rhythm type. For stable patients, the approach is to determine whether the complex is narrow or wide and whether the rhythm is regular or irregular.

### Classification Framework

Narrow-complex tachycardia (QRS less than 120 ms) originates above the ventricles. If regular, consider sinus tachycardia, SVT (AVNRT or AVRT), or atrial flutter. If irregular, consider atrial fibrillation, multifocal atrial tachycardia, or atrial flutter with variable block. Wide-complex tachycardia (QRS 120 ms or greater) should be assumed to be ventricular in origin until proven otherwise. Regular wide-complex tachycardia includes ventricular tachycardia, SVT with aberrant conduction, or SVT with a pre-existing bundle branch block. Irregular wide-complex tachycardia includes polymorphic VT, atrial fibrillation with aberrancy, or AF with pre-excitation (WPW) — the last being a life-threatening emergency.

| QRS Width | Regularity | Differential Diagnosis |
|---|---|---|
| Narrow (< 120 ms) | Regular | Sinus tachycardia, AVNRT, AVRT, atrial flutter |
| Narrow (< 120 ms) | Irregular | Atrial fibrillation, MAT, atrial flutter with variable block |
| Wide (≥ 120 ms) | Regular | VT, SVT with aberrancy, SVT with pre-existing BBB |
| Wide (≥ 120 ms) | Irregular | Polymorphic VT, AF with aberrancy, AF with WPW |

## Supraventricular Tachycardia (SVT)

### AVNRT (AV Nodal Reentrant Tachycardia)

AVNRT is the most common type of paroxysmal SVT, accounting for approximately 60 percent of cases. It involves a reentrant circuit within or adjacent to the AV node using dual AV nodal pathways. The typical rate is 150 to 250 bpm with a narrow complex and regular rhythm. P-waves are usually buried within the QRS complex or appear as a pseudo-R-prime deflection in V1 and a pseudo-S wave in inferior leads. Onset and offset are characteristically abrupt.

### AVRT (AV Reciprocating Tachycardia)

AVRT uses a reentrant circuit that includes an accessory pathway (bypass tract). Orthodromic AVRT, the most common form, conducts anterograde through the AV node and retrograde through the accessory pathway, producing a narrow complex. Antidromic AVRT conducts in the opposite direction and produces a wide complex. AVRT is associated with Wolff-Parkinson-White (WPW) syndrome.

### Management of SVT

The first-line intervention is vagal maneuvers. The modified Valsalva technique (REVERT) involves sustained strain for 15 seconds in a semi-recumbent position, followed by immediately lowering the patient supine with passive leg raise — this achieves a conversion rate of approximately 43 percent compared to 17 percent for standard Valsalva. Carotid sinus massage is an alternative but should be avoided in patients with a carotid bruit or stroke history. Facial cold water immersion (the diving reflex) is especially effective in pediatric patients.

If vagal maneuvers fail, adenosine is second-line. The dose is 6 mg by rapid IV push with an immediate 20 mL normal saline flush, followed by 12 mg if there is no response (which can be repeated once). It must be given through a proximal IV (antecubital or above) with a rapid push technique because its half-life is less than 10 seconds. Adenosine produces transient AV block that terminates reentrant circuits using the AV node. Side effects include chest tightness, flushing, dyspnea, and transient asystole — patients should be warned. Adenosine is safe in pregnancy. The dose should be reduced by 50 percent if given through a central line or if the patient is taking dipyridamole or carbamazepine, and increased for patients using theophylline or caffeine. It is also diagnostically useful, as it may unmask atrial flutter or other atrial tachycardias by producing transient AV block.

If adenosine fails, calcium channel blockers such as diltiazem (0.25 mg/kg IV over 2 minutes) are the next option. Synchronized cardioversion at 50 to 100J biphasic is reserved for refractory cases.

### WPW Considerations

WPW is identified on resting ECG by a delta wave — a slurred upstroke of the QRS caused by pre-excitation via the accessory pathway. The life-threatening scenario is atrial fibrillation with WPW, which produces an irregularly irregular wide-complex tachycardia. AV nodal blocking agents — adenosine, diltiazem, beta-blockers, and digoxin — are absolutely contraindicated in this setting because they can cause unopposed conduction down the accessory pathway, leading to ventricular fibrillation. Treatment is procainamide or cardioversion.

## Atrial Fibrillation

### Pathophysiology

Atrial fibrillation arises from chaotic electrical activity originating from pulmonary vein foci. It produces an irregularly irregular rhythm with no discernible P-waves and variable R-R intervals. It is classified by duration: paroxysmal (less than 7 days), persistent (more than 7 days), long-standing persistent (more than 1 year), and permanent.

### Rate Control

The target heart rate is below 110 bpm at rest, based on the RACE II trial, which showed that lenient rate control is as effective as strict control targeting below 80 bpm. Diltiazem (0.25 mg/kg IV bolus, repeated at 0.35 mg/kg in 15 minutes if needed, then infusion at 5-15 mg/hr) is the most effective single agent for rapid rate control but should be avoided in HFrEF due to negative inotropy. Metoprolol (5 mg IV every 5 minutes up to 15 mg) is less effective alone but is preferred in HFrEF. Amiodarone (150 mg IV over 10 minutes, then 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours) is useful when rate control agents are limited by hypotension or heart failure and provides both rate and rhythm control. Digoxin (0.25-0.5 mg IV) has a slow onset of 4 to 6 hours and serves as an adjunct in HFrEF.

### Rhythm Control (ED Cardioversion)

The Ottawa Aggressive Protocol supports ED cardioversion of recent-onset AF (less than 48 hours). Pharmacologic cardioversion with procainamide (15-17 mg/kg IV over 30-60 minutes) is attempted first, followed by electrical synchronized cardioversion at 200J biphasic if drugs fail. The success rate exceeds 90 percent for recent-onset AF, and patients can be safely discharged the same day with a short-term antiarrhythmic and anticoagulation. Cardioversion criteria require that the duration is clearly less than 48 hours, the patient is hemodynamically stable, and there is no structural heart disease. If the duration exceeds 48 hours or is uncertain, rate control with anticoagulation is the appropriate approach, with TEE-guided cardioversion or 3 to 4 weeks of anticoagulation before elective cardioversion.

### Stroke Risk and Anticoagulation

The CHA2DS2-VASc score guides long-term anticoagulation decisions. Points are assigned for congestive heart failure (1), hypertension (1), age 75 or older (2), diabetes (1), stroke or TIA (2), vascular disease (1), age 65-74 (1), and female sex (1). Anticoagulation is recommended for scores of 2 or higher in males and 3 or higher in females. DOACs are preferred over warfarin for nonvalvular AF. ED-initiated anticoagulation for new AF is appropriate when the score indicates need.

| CHA₂DS₂-VASc Component | Points |
|---|---|
| **C**ongestive heart failure | 1 |
| **H**ypertension | 1 |
| **A**ge ≥ 75 | 2 |
| **D**iabetes | 1 |
| **S**troke / TIA | 2 |
| **V**ascular disease | 1 |
| **A**ge 65–74 | 1 |
| **Sc** (Sex category — female) | 1 |

### Atrial Flutter

Atrial flutter produces a regular atrial rate of approximately 300 bpm with characteristic sawtooth flutter waves best seen in leads II, III, aVF, and V1. With typical 2:1 conduction, the ventricular rate is 150 bpm — any regular tachycardia at exactly 150 bpm should be considered atrial flutter until proven otherwise. Variable block produces an irregular ventricular response. Rate control is more difficult than in AF and may require cardioversion. Anticoagulation guidelines are the same as for AF.

## Wide-Complex Tachycardia

### VT vs. SVT with Aberrancy

The default assumption for any wide-complex tachycardia should be ventricular tachycardia — VT is both more common and more dangerous. Treating SVT as VT is safe, but treating VT as SVT can be fatal.

### ECG Criteria Favoring VT

AV dissociation is the most specific finding — P-waves marching through at an independent rate from the QRS complexes. Capture beats (narrow complex beats from a conducted sinus impulse) and fusion beats (hybrid morphology between sinus and ventricular beats) also favor VT. A very wide QRS (greater than 160 ms), northwest axis (extreme right axis deviation), and concordance (all precordial leads positive or all negative) are additional supporting features. The Brugada criteria, Vereckei algorithm, and Sasaki rule are systematic approaches to differentiation.

### Monomorphic VT Management

Hemodynamically unstable monomorphic VT requires synchronized cardioversion at 100 to 200J biphasic. For stable monomorphic VT, pharmacologic options include amiodarone (150 mg IV over 10 minutes, most commonly used), procainamide (15-17 mg/kg IV at 20-50 mg/min, often preferred but slower; monitor for QRS widening and hypotension), and lidocaine (1-1.5 mg/kg IV push, faster onset but less effective overall). Cardioversion is used if medications fail.

### Polymorphic VT

Polymorphic VT with a normal QTc is treated as ischemia-driven VT with amiodarone, treatment of underlying ischemia, and cardioversion. Polymorphic VT with a prolonged QTc — Torsades de Pointes — requires a fundamentally different approach. IV magnesium (2 g over 1-2 minutes) is first-line. Overdrive pacing via transvenous pacing or isoproterenol infusion shortens the QT interval by increasing the heart rate. Amiodarone, procainamide, and sotalol are contraindicated because they further prolong the QT interval and worsen Torsades. The underlying cause must be identified and corrected: offending drugs (antiarrhythmics, antipsychotics, antibiotics) and electrolyte abnormalities (hypokalemia, hypomagnesemia).

### Pulseless VT / VF

Pulseless VT and VF are treated with unsynchronized defibrillation per ACLS protocol, with epinephrine and amiodarone per the algorithm.

<image>A 12-lead ECG teaching panel showing four different tachyarrhythmias side by side for comparison. Panel A: AVNRT showing narrow complex regular tachycardia at 180 bpm with pseudo-R-prime in V1 and pseudo-S in lead II. Panel B: Atrial fibrillation with irregularly irregular narrow complex rhythm with no P-waves. Panel C: Atrial flutter with 2:1 block showing sawtooth flutter waves at 300 bpm with ventricular rate 150. Panel D: Monomorphic ventricular tachycardia showing wide complex regular tachycardia at 170 bpm with AV dissociation marked by arrows pointing to independently marching P-waves.</image>

<image>A step-by-step illustration of the modified Valsalva maneuver (REVERT technique). Four sequential panels show: (1) Patient seated semi-recumbent at 45 degrees blowing into a 10 mL syringe for 15 seconds. (2) Patient immediately lowered to supine position. (3) Passive leg raise to 45 degrees for 15 seconds by the clinician. (4) Patient returned to semi-recumbent position with a rhythm strip below showing conversion from SVT to normal sinus rhythm. Success rate annotation shows 43% vs 17% for standard Valsalva.</image>

## Clinical Pearls

Any regular narrow-complex tachycardia at exactly 150 bpm is atrial flutter until proven otherwise. Wide-complex tachycardia is VT until proven otherwise — never give calcium channel blockers or adenosine empirically for wide-complex tachycardia. The modified Valsalva (REVERT technique) more than doubles SVT conversion rates compared to standard Valsalva and should be taught to patients with recurrent SVT. AF with WPW (pre-excited AF) is an AV nodal blocker-free zone — only procainamide or cardioversion should be used. Adenosine is safe in pregnancy and diagnostically useful for unmasking atrial flutter or other atrial tachycardias. Torsades de Pointes requires magnesium and overdrive pacing — amiodarone and procainamide are contraindicated. Rate control to below 110 bpm is sufficient in atrial fibrillation based on the RACE II trial, and aggressive rate control to below 80 bpm offers no additional benefit. The Ottawa Aggressive Protocol allows safe same-day cardioversion and discharge for recent-onset AF (less than 48 hours) with greater than 90 percent success.

## References

- Appelboam A, et al. REVERT Trial: Modified Valsalva manoeuvre in supraventricular tachycardia. *Lancet*. 2015;386:1747-1753.
- Stiell IG, et al. Ottawa Aggressive Protocol for acute atrial fibrillation/flutter. *CJEM*. 2010;12:181-191.
- Van Gelder IC, et al. RACE II: Lenient versus strict rate control in atrial fibrillation. *NEJM*. 2010;362:1363-1373.
- January CT, et al. 2019 AHA/ACC/HRS Focused Update on Atrial Fibrillation. *J Am Coll Cardiol*. 2019;74:104-132.
- Brugada P, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. *Circulation*. 1991;83:1649-1659.