Multiple types of narrow complex tachycardia (NCT) are encountered in the acute care setting, the vast majority of which originate above the ventricles and have a rate over 100 bpm with a QRS complex duration less than 120 ms; the single exception to this statement is the ventricular‐based NCT called fascicular tachycardia or fascicular ventricular tachycardia – this rhythm is quite rare and is usually encountered in medication toxicity presentations. Any tachycardic rhythm originating above the ventricles is technically a supraventricular tachycardia (SVT); thus the term SVT is a general category of tachydysrhythmias. A distinction must be made between SVT and paroxysmal supraventricular tachycardia (PSVT); PSVT is a commonly used term to describe a specific type of NCT with an abrupt onset and resolution. Most of the NCTs described below tend to be regular, with the exception of atrial fibrillation and multifocal atrial tachycardia (MAT).

The differential diagnosis of the NCT (Table 22.1) includes sinus tachycardia, atrial fibrillation, atrial flutter, PSVT, MAT, and paroxysmal atrial tachycardia (PAT). In addition, the Wolff–Parkinson–White syndrome can present with a NCT similar in appearance to PSVT. Lastly, the rare fascicular ventricular tachycardia should also be considered in the differential diagnosis of the NCT.

Sinus tachycardia is a common finding in response to physiologic stress and is identified on the electrocardiogram (ECG) (Figure 22.1) by a regular NCT with identical, upright P wave for each QRS complex; importantly, the P waves are upright in leads I, II, and III. Sinus tachycardia has both a gradual onset and a gradual “termination.” Rates range from 100 to approximately 160 bpm in the adult; age‐related rates are seen in children, with maximum rates approaching 200 bpm in the infant and young child. Sinus tachycardia should be considered a “reactive rhythm” in that it is usually secondary to a primary physiologic event such as hypovolemia, hypoperfusion, hypoxia, fever, pain, anxiety, and medication effect (Clinical Presentation Box 22.1). Treatment is rarely required for the tachycardia itself; rather, attention and potential therapy should be paid to the cause of the sinus tachycardia (Management Box 22.1).

Atrial fibrillation is a result of multiple ectopic foci in the atrium firing simultaneously at atrial rates of up to nearly 600 bpm. When an occasional impulse reaches the atrioventricular (AV) node, conduction of a ventricular impulse occurs. The resulting ventricular rate is very irregular and can range from severely bradycardic to extremely tachycardic with rates up to 150–250 or even higher in the presence of accessory AV tracts (i.e. the Wolff–Parkinson–White syndrome). The usual rate of atrial fibrillation without medication effect or other active disease impact is approximately 170 bpm. ECG (Figure 22.2) tracings reveal absent P waves and a chaotic (wavy, bumpy) baseline caused by the multiple small atrial firings. The QRS complex is narrow except at extreme high rates or in patients with coexistent intraventricular conduction delays or accessory pathways (APs). Importantly, the rhythm pattern is irregular in an irregular fashion, thus the irregularly irregular pattern of atrial fibrillation (Management Box 22.2).

Atrial flutter is caused by rapid firing of a single, ectopic atrial focus that is continuously restimulated by an aberrant reentry loop within the atrium. The atrial rate is generally 250–350 bpm with only a portion of these atrial impulses proceeding through the AV node to cause ventricular depolarization. The ventricular rate depends on the ratio of atrial impulses generated to ventricular impulses sensed. Commonly, atrial flutter is seen with 2 : 1 atrioventricular (A : V) conduction causing a regular NCT with a rate of approximately 150 bpm (Clinical Presentation Box 22.2). The ECG (Figure 22.3) demonstrates regular, identical “flutter” waves (the P waves) which appear as pointed, asymmetric structures. With 2 : 1 block, there will be two flutter waves for every one generated QRS. If uncertain whether flutter waves are present, performing vagal maneuvers may momentarily slow the A : V conduction to 3 : 1 (ventricular rate of 100 bpm) or 4 : 1 (ventricular rate of 75 bpm), thus making the flutter waves more apparent. The clinician should consider atrial flutter (Figure 22.3) in patients with NCT and fixed (i.e., non‐varying) ventricular rates of approximately 150 bpm.