HR>100 with a QRS duration <0.12 sec (120 ms), can be regular or irregular. Given their narrow QRS duration they originate above the ventricle and are commonly referred to as a supraventricular tachycardia (SVT). An SVT may also have a wide QRS when there is aberrant conduction. Tachycardia is classified according to whether: regular or irregular, narrow complex or wide complex.

* Atrial activity on EKG

• Sinus tachycardia
• Atrial tachycardia
• Atrial flutter with regular block
• Atrial activity might be buried on EKG
• A-V nodal reentry (AVNRT)
• Accessory-pathway mediated reentry (aka: AVRT, Wolf-Parkinson-White)
• No atrial activity on EKG
• Junctional tachycardia

</WRAP> | <WRAP>

• Atrial Fibrillation
• Atrial Flutter with variable block
• Multifocal atrial tachycardia (MAT)
• Frequent premature atrial complexes (PACs)

</WRAP> |

• Obtain 12-lead ECG and full set of vital signs to determine hemodynamic stability.
• If unstable or showing signs of rate related cardiovascular compromise (chest pain, altered mental status, hypotension or other signs of shock), follow ACLS unstable SVT protocols.
• Compare current ECG to prior 12-lead ECG. Remember to evaluate for evidence of delta waves (WPW) when at a slower rate as this will effect management (see below).

• lf unstable, follow ACLS protocol and do not delay synchronized cardioversion.
• Tailor treatment to the type of narrow complex tachvcardia (see below).
• To break an SVT, can try vagal maneuvers or adenosine:
• Vagal maneuvers: Can often break SVT
  • Types: cough or bear down as if to have a bowel movement.
  • Carotid Massage: stimulates baroreceptors that trigger a reflexive increase in vagal activity and slowing conduction through the AV node. Place firm pressure to the neck at the level of the cricoid cartilage for 5 sec with circular motion. Prior to doing so, auscultate for carotid bruits, if present do not perform this procedure.
• Adenosine:
  • Warn patients that adenosine will make them feel terrible but it will be short (a few seconds).
  • Dosing and administration
  • Peripheral IV: 6mg X1, may repeat X1 6mg dose several minutes later if not broken, then increase to 12mg dose X1
  • Central Line: lower doses of 3mg with a repeat dose and then increased dose of 6mg.
  • Continuous ECG monitoring during administration.
  • Rapid IV flush is required due to very short half-life.
  • Adverse Reactions: bronchospasm, ventricular fibrillation (VF, very rare), chest pain and dyspnea (more common).
• 60-80% of patients treated with a 6mg dose of adenosine will break their SVT and 90-95% will break with a dose of 12mg.
• If the rhythm doesn’t break, it often will slow it enough to reveal the underlying rhythm such as atrial flutter or atrial tachycardia.
• AVOID IN: severe COPD
• DO NOT USE IN: Heart transplant recipients (causes prolonged asystole), wide complex tachycardia (unless SVT with aberrancy is certain, causes VF), and WPW (causes rapid ventricular rate and can degrade to VF, treat with procainamide if occurs), previous allergy.
• Rate control agents: see Cardiology: Atrial fibrillation.

• Sinus tachycardia (ST): When cardiac function is compromised the cardiac output may be dependent on

the HR due to a fixed stroke volume (SV).

• Causes: physiologic response to a stress on the body and is often the marker of an underlying illness:
  • infection, fever, pain, hypovolemia, hypotension
  • Pulmonary embolism, hypoxia
  • Cardiac tamponade, pericarditis
  • Metabolic conditions: hyperthyroidism
  • Alcohol withdrawal
  • Response to sympathomimetic drugs (i.e.: vasopressors, bronchodilators, beta agonists)
• Diagnosis: p-waves on EKG and during adenosine push. Upright in leads | and II, downward in aVR. Maximum HR of a normal individual is 220 minus age.
• Treatment: treat the underlying cause. Generally do not beta block.
• Atrial tachycardia (AT):
• Causes: paroxysmal in nature and is caused by a focus of enhanced automaticity within the atria or a focus of an ectopic atrial pacemaker.
• Diagnosis: Can be difficult to diagnose. Rate usually <250bpm, will have non-sinus p-waves on rhythm strip and may require adenosine (see below) to diagnose. Onset is typically with an premature atrial contraction (you may see a deformed T-wave which reflects a P-wave superimposed on the T-wave.
• Atrial flutter with regular block:
• Causes: reentrant circuit within atrium.
• Diagnosis: classic “saw-tooth” p-wave which typically has a rate of ~300 bpm (range 170 bpm-320 bpm). The ventricular rate is determined by the rate of conduction block (often 2:1 (150 bpm). Slowing of the atrial flutter rate (down to 170 bpm) can be seen when patients are on amiodarone or other anti-arrhythmics.
• A-V nodal reentry tachycardia (AVNRT):
• Causes: dual conduction pathway within the A-V node itself, typically one that conducts fast and one that conducts slowly. AVNRT is usually set off by a premature atrial contraction (PAC).
• Diagnosis: Retrograde P waves can be buried within the QRS complex OR create S-waves in inferior leads (pseudo-S waves) and apparent R waves in V1 (pseudo-R’). Typically have a short RP interval). HR is typically 180 +/- 20 bpm.
• Treatment: AV nodal blockade (carotid sinus massage, adenosine to break the cycle, beta blockers, calcium channel blockers). If unstable or symptomatic, cardiovert.
• A-V reentry tachycardia (AVRT):
• Causes: an SVT that is generated by an accessory pathway. A common example is Wolf-Parkinson-White (WPW) syndrome.
• Diagnosis: short RP interval, but longer than the RP in AVNAT, retrograde P waves.
• WPW: characterized by the presence of the delta wave, which is a broadened up sloping of the R wave.
• Treatment: AV nodal blockade as above. In contrast to patients with atrial fibrillation and WPW,

adenosine can be given to patients with AVRT.

• Junctional tachycardia: Rare in adults
  • Causes: MI, digoxin toxicity, myocarditis
  • Diagnosis: rate usually 100-140 and P waves absent (buried within QRS) or seen after QRS (retrograde)
  • Treatment: treat the underlying cause.

• Atrial fibrillation: see Cardiology: Atrial fibrillation for details
  • Causes: very common in acutely ill patients, especially older individuals.
  • Diagnosis: lack of p-waves or flutter waves in all leads, irregularly irregular rhythm.
  • Treatment: treat this like sinus tachycardia - treat the underlying cause (sepsis, volume overload)! In general, do not rate or rhythm control atrial fibrillation unless it is causing hemodynamic significance. In which case try low-dose metoprolol or diltiazem IV, or amiodarone bolus and drip. Cardiovert if unstable.
• Atrial flutter with variable AV block:
  • Causes: same as atrial fibrillation
  • Diagnosis: will look similar to AF except with the presence of flutter waves. Often the flutter waves will be visible in the inferior leads with a rate of ~300 bpm.
  • Treatment: as above but very difficult to rate control. More responsive to EP ablation than atrial fibrillation

and can often be cured.

• Multifocal atrial tachycardia (MAT):
  • Causes: multiple ectopic atrial pacemakers, usually associated with pulmonary disease, also can be seen in underlying ischemic cardiac disease, hypomagnesemia, hypokalemia.
  • Diagnosis: at least 3 morphologically distinct p waves with differing PR intervals on ECG.
  • Treatment: treat the underlying cause, no role for AV nodal blockade, but verapamil may be useful to eliminate the multifocal atrial rhythm.
• Frequent PACs: usually benign

• Sinus tachycardia is usually not treated and is a signal for an underlying problem.
• Synchronized cardioversion and ACLS protocol for unstable SVT should not be delayed.
• Adenosine makes patients feel terrible, be aware.
• Adenosine is both diagnostic and therapeutic; always use continuous ECG monitoring during administration.
• In patients with atrial fibrillation with a pre-excitation pathway (look for delta waves), avoid adenosine, which can precipitate VT or VF.
• Atrial flutter can often be very difficult to rate control.