The AHA Guidelines and Scientific Statements Handbook

Chapter 16 Supraventricular Arrhythmias

Table 16.1 Recommendations for acute management of hemodynamically stable and regular tachycardia

ECG Recommendation* Classifi cation Level of evidence

Narrow QRS complex tachycardia (SVT) Vagal maneuvers I B
Adenosine I A
Verapamil/diltiazem I A
Beta-blockers IIb C
Amiodarone IIb C
Digoxin IIb C

Wide QRS complex tachycardia

• SVT + BBB See above


• Preexcited SVT/AF Flecainide‡ I B
  Ibutilide‡ I B
  Procainamide‡ I B
  DC cardioversion I C


• Wide QRS complex tachycardia of unknown origin Procainamide‡ I B
  Sotalol‡ I B
  Amiodarone I B
  DC cardioversion I B
  Lidocaine IIb B
  Adenosine§ IIb C
  Beta-blockers¶ III C
  Verapamil** III B


• Wide QRS complex tachycardia of unknown origin in patients with Amiodarone I B
  poor LV function DC cardioversion, I B
  Lidocaine I B

The order in which treatment recommendations appear in this table within each class of recommendation does not necessarily refl ect a preferred sequence of
administration.

• All listed drugs are administered intravenously.
  ‡ Should not be taken by patients with reduced LV function.
  Adenosine should be used with caution in patients with severe coronary artery disease because vasodilation of normal coronary vessels may produce ischemia in
  vulnerable territory. It should be used only with full resuscitative equipment available.
  ¶ Beta blockers may be used as fi rst-line therapy for those with catecholamine-sensitive tachycardias, such as right ventricular outfl ow tachycardia.
  ** Verapamil may be used as fi rst-line therapy for those with LV fascicular VT.
  AF indicates atrial fi brillation; BBB, bundle-branch block; DC, direct current; ECG, electrocardiogram; LV, left ventricular; QRS, ventricular activation on ECG; SVT,
  supraventricular tachycardia; VT, ventricular tachycardia.

management of hemodynamically stable and regular
tachycardia are shown in Table 16.1 [2–4].

Specifi c arrhythmias

Sinus tachyarrhythmias
Physiological sinus tachycardia
Sinus tachycardia is defi ned as an increase in sinus
rate to more than 100 bpm in response to physical,

emotional, pathological, or pharmacological stress.

It is nonparoxysmal, thus differentiating it from re-

entry. The P waves are positive in leads I–II and aVF,

and negative in AVR. The frontal plane axis is

between 0 and +90, and can be negative in leads V1

and V2 but positive in leads V3 to V6. Several patho-

logical conditions may cause sinus tachycardia

including pyrexia, hypovolemia, anemia, or certain

drugs (salbutamol, aminophylline, atropine,