I. Problem/Condition.

Tachycardias include all heart rhythms with a rate > 100 bpm. They can be divided into two primary categories:

  • ) Narrow Complex Tachycardias (NCT) which have a QRS duration < 120 msec
  • ) Wide Complex Tachycardias (WCT) which have a QRS duration > 120 msec

The NCT’s are due to rapid activation of the ventricles via the normal intrinsic conduction system, thus originate at or above the atrioventricular (AV) node.

WCT’s have a wide QRS reflecting a slow or abnormal path of ventricular activation. They may originate from one of three places: outside the intrinsic conduction pathway (ventricular tachycardia), as a supraventricular tachycardia with a bundle branch block or aberrancy, or as a supraventricular tachycardia with AV conduction over an accessory pathway.

Common Mechanisms of Tachycardias

There are two primary mechanisms that drive tachycardias:

  • ) abnormal impulse generation (automaticity) and
  • ) abnormal impulse propagation (reentry)

Enhanced automaticity can occur either spontaneously or be triggered by a stimulus, the latter of which is much less common. The cardiac cells with the potential for enhanced automaticity have enhanced phase 4 depolarization and therefore may depolarize at a rate faster than the pacemaker cells. These are often referred to as the “latent pacemakers” of the heart. If the rate of firing in these latent pacemaker cells exceeds that of the sinus node, they become the predominant pacemaker. Some of the more common causes of increased automaticity include catecholamine surge (pain, exercise), hypoxemia, ischemia, hypokalemia, and stretch on the heart. The triggered form of automaticity is relatively rare but can occur with antiarrhythmic medications.

Reentry is by far the more common mechanism underlying tachycardias. In areas of the heart prone to reentry, there are several pathways that conduct with slightly different conduction properties. When a premature beat occurs, it exaggerates the difference between the two pathways. It may find one pathway refractory, thereby setting the stage for a short circuit (repetitive excitation of a region of the heart) that perpetuates the arrhythmia.

II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

The differential diagnosis for any tachycardia begins with a review of a 12 lead EKG taken during the arrhythmia. From there, the differential is best categorized first by the width of the QRS. SeeFigure 1

Figure 1
Guidelines for Management of patients with supraventricular arrhythmias-executive summary, 1493-1531, 2003, with permission from Elsevier.

Narrow Complex Tachycardias: If the QRS is < 120 msec, the specific diagnosis is best made by dividing the tachycardias into those that are irregular and those that are regular rhythms.

A)Irregularly Irregular rhythm

  • Atrial Fibrillation
  • Multifocal Atrial Tachycardia
  • Atrial flutter with variable block/conduction

B)Regular rhythm

  • Sinus Tachycardia
  • Atrial Tachycardia
  • Atrial Flutter with 2:1 block, or constant block
  • AV nodal Reentrant Tachycardia
  • AV Reentrant Tachycardia
  • Accelerated Junctional Tachycardia

Wide Complex Tachycardias:If the QRS is > 120 msec, the vast majority of the time the rhythm is due to one of three possibilities:

  • ventricular tachycardia (the most common – usually has a QRS > 140 msec)
  • supraventricular tachycardia with aberrancy (LBBB, RBBB, accessory pathway)

Unfortunately, ventricular tachycardias can be regular or irregular so the RR interval often does not help to make the diagnosis. A careful review of the patient’s comorbidities may provide some insight, however. Patients with ischemic heart disease, scar, systolic dysfunction and underlying conduction abnormalities are more likely to present with ventricular tachycardia.

Atrial Fibrillation
  • Multiple Reentrant wavelets
  • Irregularly irregular
  • No p waves present (coarse atrial fibrillation may mimic p waves)
  • Narrow, unless aberrancy
  • Atrial rate; 400-700 bpm, ventricular response usually 100-200 bpm
  • Slow ventricular response (<100 bpm) may occur with antiarrhythmics, high vagal tone, conduction disease
  • Extreme RVR (>200 bpm) may occur with catecholamine excess, thyroid disease, accessory pathway
  • Ashmann phenomenon: short RR after long RR may result in a wide complex beat (of RBBB morphology)
Multifocal Atrial Tachycardia
  • Enhanced automaticity of multiple atrial foci (>= 3 atrial foci)
  • Rate 100-180 bpm
  • Irregularly Irregular
  • Narrow unless aberrant pathway
  • Multiform p waves (>= 3 morphologies) with isoelectric baseline inbetween
  • Usually occurs with hypoxia/hypercapnea, but also consider hypokalemia, hypomagnesemia, sympathomimetic drugs, infection
Atrial Flutter
  • Reentry within atrium
  • Atrial rate 270-300 bpm, ventricular response may be 1:1, 2:1, 3:1, although slower atrial and ventricular rates have been seen with underlying conduction or structural heart disease
  • Regular atrial activation in a sawtooth pattern (flutter waves)
  • Narrow complex, unless aberrancy
  • Paroxysmal
Sinus Tachycardia
  • Automaticity drives this rhythm
  • P waves precede each QRS, and are upright in II and aVF
  • Narrow unless aberrancy
  • Regular
  • Maximum rate dependent on age: ~200 – 0.5 x age
  • Gradual variations: “ramps’ up and down
  • Treat underlying condition
  • Inappropriate sinus tachycardia can occur resulting in a increased HR unrelated to, or out of proportion to, a stressor
Atrial Tachycardia
  • Uncommon but more often seen in patients with underlying cardiac abnormalities
  • Reentrant arrhythmias or arrhythmias arising in an ectopic foci of the atria that is not the sinus node
  • Paroxysmal palpitations with sudden onset and termination
  • Regular or irregular
  • Narrow unless aberrancy
  • Single P wave morphology which are visible before each QRS but have a different morphology than the sinus P wave (and may even be negative if low in the atrium)
  • Rates 100-250 bpm
AV Nodal Reentrant Tachycardia
  • Most common reentrant rhythm
  • Referred to as a “paroxysmal supraventricular tachycardia” as it has sudden onset and termination
  • Regular
  • Usually no p waves visible OR visible as a pseudo-R wave in lead V1
  • Rates 140-200 bpm
  • More common in women and not associated with structural heart disease
  • Narrow unless aberrancy
AV Reentrant Tachycardia

Reentrant rhythm via an accessory pathway or bypass tract outside the AV node

Referred to as a “paroxysmal supraventricular tachycardia” as it has sudden onset and termination


Rates 140-240 bpm

P wave often present in the ST segment but separted from the QRS by 70 ms

Narrow or wide: narrow if orthodromic conduction (more common) and wide if antidromic conduction

Accelerated Junctional Tachycardia
  • Uncommon in adults
  • Enhanced automaticity: beat to beat variability +/- gradually “ramps’ up or down
  • Narrow unless aberrancy
  • Regular
  • Rate: 70-130 bpm
  • 1:1 AV association
  • Negative p waves after QRS reflecting retrograde conduction
  • Think catecholamine excess: Mi/ischemia, infection, cardiomyopathy
  • Can occur with digoxin toxicity
Ventricular Tachycardia
  • Wide QRS, usually QRS> 140 msec
  • Reentrant, usually triggered by PVC
  • Monomorphic or polymorphic
  • Rate: 140-220 bpm
  • Regular or irregular
  • P waves may be retrograde conducted or visible but dissociated from the ventricle
  • Most commonly occurs in structurally abnormal hearts
  • > 30 seconds of consecutive beats = sustained VT

B. Describe a diagnostic approach/method to the patient with this problem.

There are four essential questions when faced with a patient with a tachycardia.

1) Is the patient stable or unstable?

The first priority with any tachycardia is to assess whether the patient has any serious signs or symptoms related to the tachycardia? These include:

  • Ischemic chest pain (usually demand ischemia, but must rule out ACS)
  • Dyspnea (rales? new onset congestive heart failure?)
  • Decreased level of consciousness (dizziness? poor cerebral perfusion?)
  • Cardiogenic shock or hypotension (cool and clammy?)

If the patient isunstable, the rhythm may require immediate management most likely with synchronized cardioversion or defibrillation.

If these signs and symptoms are due to something other than the arrhythmia (sepsis, hemorrhage, pulmonary embolism, tamponade, dehydration, etc) then treat the underlying problem rather than the arrhythmia.

If the patient isstable, then there is time to obtain a specific diagnosis and assess for systolic dysfunction as this may increase risk in your patient and alter your therapy.

2) Is the rhythm wide or narrow?

Whenever possible, a 12 lead EKG should be performed during the tachycardia episode as long as it does not delay immediate therapy.

  • If the QRS is narrow, then the tachycardia is almost always suprventricular and go on to #3.
  • If the QRS is wide, then you must consider one of two possibilities: ventricular tachycardia or supraventricular tachycardia with aberrancy (LBBB, RBBB, accessory pathway.)

3) Are there P waves?

If so,

  • Are they associated with each QRS complex,
  • Are they before or after the QRS complex, and
  • Are they positive or negative?

4) Is the rhythm regular, regularly irregular, or irregularly irregular?

Irregularly irregular:

  • If narrow complex, and there are no apparent P waves present, and the RR interval is irregular =Atrial Fibrillation
  • If narrow complex, and there are multiple P wave morphologies (>3), and the RR interval is irregular =Multifocal Atrial Tachycardia (MAT)

Regular +/- Regularly Irregular (couplet beating may be present):

  • If narrow complex, and there are p waves indicating an atrial rate faster than the ventricular rate with regularly irregular RR intervals OR regular RR intervals at 1:1, 2:1, or 3:1 A:V rate =atrial flutter


  • If narrow complex, and a P wave precedes each QRS, and the RR interval is regular =sinus rhythm
  • If narrow complex, and there are no apparent P waves present or present as a pseudo R wave in V1, and the RR interval is regular =AV Nodal Reentrant Tachycardia (AVNRT)
  • If narrow complex, and the P wave is visible in the ST segment and separated from the QRS by 70 ms, and the RR interval is regular =AV Reentrant Tachycardia (AVRT)
  • If narrow complex, and the RP > PR, and the RR interval is regular =Atypical AVNRT or Atrial Tachycardia (AT)
  • If narrow complex, and the P waves are negative and follow the QRS =Accelerated Junctional Tachycardia

Wide Complex:

  • If wide complex, and P waves are visible but not clearly associated with the QRS (AV dissociation), and the ventricular rate is faster than the atrial rate, this is pathognomonic forVT. Unfortunately, this is only present in 30% of all VT’s.
  • Although VT can be regular or irregular, always consider atrial fibrillation with aberrancy if presented with an irregularly irregular wide complex tachycardia
  • Underlying heart disease favors VT over a SVT with aberrancy

5) Is it responsive to adenosine?

Adenosine is a medication that can be diagnostic, therapeutic or both.

It breaks the rhythm where the AV node is part of the entry circuit

  • PSVT due to AV node reentry
  • PSVT due to reentry involving accessory pathway

It transiently slows a rhythm that originates above the AV node:

  • Those due to enhanced automaticity: MAT and sinus tachycardia
  • Those due to reentry circuit in the atrium: atrial flutter and atrial fibrillation


Half life: 10-30 seconds

Rapidly metabolized

Inhibits AV node

Very transient side effects: dyspnea, flushing and chest pain

Contraindications: asthma, sick sinus syndrome, 2nd or 3rd degree block, heart transplant patients

Dose: 6 mg IV rapid bolus then NS flush, redose with 12mg IV if not effective

1. Historical information important in the diagnosis of this problem.

Unfortunately, most patients are asymptomatic at the time of an evaluation for an arrhythmia. If the arrhythmia occurs in the hospital, and preferably on telemetry, the diagnosis becomes more straightforward. Symptoms occurring at the time of an arrhythmia are critical. Some of the more common complaints include palpitations, lightheadness/dizziness, dyspnea, chest discomfort, flushing, presyncope and rarely syncope.

It is often helpful to ascertain whether the symptoms have an abrupt onset and termination, whether they are regular or irregular, the number of episodes and their duration, and activities that provoke symptoms. For example, patients with sinus tachycardia warrant a deeper look into underlying infection, hyperthyroidism, stress/anxiety, medications or dehydration/bleeding. Patients who are able to terminate symptoms with vagal maneuvers are most often describing a PSVT such AVNRT or AVRT. Patients with complaints of dyspnea or a history of lung disease may describe symptoms of MAT.

Finally, patients with a positive family history of sudden cardiac death should be treated seriously. This is a strong predictor of susceptibility to ventricular arrhythmias and sudden death. A thorough drug history, both prescribed and not prescribed medications including dosages, should be obtained.

Syncope or severe symptoms occurring with palpitations, should always result in a formal cardiac workup.

Syncope only occurs in about 15% of patients with SVT. Usually syncope does not result from the tachycardia itself but from a prolonged pause that can occur after abrupt termination of the tachycardia. Syncope may also be a sign of a more serious underlying problem such as atrial fibrillation or flutter conducting down an accessory pathway or concomitant structural heart disease such as a dilated cardiomyopathy with systolic dysfunction, ischemic heart disease, valvular disease (aortic stenosis or mitral stenosis), or hypertrophic cardiomyopathy.

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

Most of the reentrant tachycardias occur in the absence of detectable heart disease. A thorough physical exam should be performed on these patients, but seldom does this alone lead to a diagnosis. If evidence for structural heart disease is found, this may aid in the final diagnosis. For example, mitral stenosis or regurgitation murmurs may point to atrial arrhythmias, and signs of congestive heart failure toward VT. One place the exam can really aid in the diagnosis is if a patient has evidence of regular cannon A waves in the jugular venous pulse during an episode of tachycardia; this may represent AV dissociation (atrial contraction against a closed tricuspid valve) that can be found in PSVT’s. Irregular cannon A waves can be seen in VT (if AV dissociation is present).

Signs of hyperthyroidism such as thyroid bruit or exophthalmos may raise the possibility of hyperthyroidism and subsequent tachyarrhythmias.

The use of vagal maneuvers (Valsalva, carotid massage, and facial immerson in cold water) can be helpful in tachycardias. Vagal stimulation can be utilized as either a diagnostic and/or therapeutic tool in patients. It is able to break a rhythm where the AV node is part of the reentry circuit: AVNRT or AVRT. It may also transiently slow a rhythm that originates above the AV node, both in rhythms that are due to enhanced automaticity (MAT, sinus tachycardia) and those with a reentry circuit that exists in the atrium (atrial flutter, atrial fibrillation), at times allowing for a clearer diagnosis.

Ventricular tachycardias will not respond to vagal stimulation and there should be no change in the rhythm when vagal stimulation is attempted in a patient.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

A resting 12 lead EKG should be performed during the arrhythmia if at all possible. If the patient is unstable and requires cardioversion, attempts to record a rhythm strip through the defibrillator should be attempted. The EKG may provide many clues to the diagnosis, even if it does not capture the arrhythmia. It can highlight electrolyte disturbances, congenital abnormalities (familial long QT, Brugada, ARVD), underlying conduction abnormalities, previous ischemic disease or infiltrative cardiomyopathy, to name a few.

Although many of the reentrant tachycardias in younger patients occur without underlying structural heart disease, it is reasonable to obtain an echocardiographic examination in patients with documented SVT to exclude it.

Unexplained tachycardia may warrant some laboratory testing such as thyroid stimulating hormone, hemoglobin/hematocrit, serum electrolytes (particularly K and Mag levels), urine toxicology screen, and serum sympathomimetic drug levels (i.e. theophylline.)

If angina precedes or occurs with a tachycardia it is reasonable to consider risk stratification for coronary artery disease with stress testing, coronary computed tomography (CT), or direct diagnostic angiography, depending on the patient and their condition.

Magnetic resonance imaging (MRI) may be useful in patients with ventricular arrhythmias if echocardiography, alone, is unable to clearly visualize subtle abnormalities of the LV and RV (such is the case with Arrhythmogenic Right Ventricular Dysplasia (ARVD) or in the evaluation of suspected infiltrative disease.

Patients with frequent, but transient, tachycardias may best served by ambulatory 24-48 hour Holter monitoring. If a patient has less frequent tachycardic episodes (unlikely to occur in a 48 hour window) an event monitor or wearable loop recorder may be a better option. Finally, for patients with rare episodes of tachycardia but with severe symptoms (syncope leading to a head injury) may be best served by an implantable loop recorder. This option is also useful in patients with dementia or psychiatric illness who are unable to activate an event monitor. Exercise stress testing may be utilized in patients whom exercise is a trigger.

Electrophysiology testing and/or referral is essential in patients who have symptoms and Wolff-parkinson-White syndrome, NCT with drug resistance or intolerance, wide complex tachycardia of unknown origin, or syncope and underlying structural heart disease.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

See “Diagnostic Approach/Method” section.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Serial troponins are often ordered in the setting of a new presentation of tachycardia. Although ischemia can trigger both supraventricular tachycardias as well as ventricular tachycardias, ischemia generally occurs with other signs and symptoms such as chest pain or dyspnea. Without accompanying symptoms of ischemia, troponins simply are an unnecessary expense.

III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem Tachycardia with Pulse.

  • ) Confirm that the patient is having a tachyarrhythmia (HR >100 bpm). Treating an arrhythmia generally warrants a HR > 150 bpm.
  • 2) Assess/assist the patient:maintain patent airway, assist with breathing if necessary; oxygen; place on telemetry; monitor blood pressure and O2
  • 3) Persistent tachyarrhythmia causing:hypotensionacutely altered mental statussigns of shockischemic chest discomfortacute heart failure

If yes? thenSYNCHRONIZED CARDIOVERSION (don’t forget sedation). If narrow complex, can consider adenosine (6 mg IV push, 12 mg IV push, or 18 mg IV push)

If no? Go to#4

4) Wide QRS (> 120 msec?)

If yes? IV access and 12 lead EKG; consider adenosine if regular and monomorphic, however, recognize that it can be potentially deleterious in a borderline stable patient due to vasodilation; consider antiarrhythmic infusion versus synchronized cardioversion; get help!

If no? IV access and 12 lead EKG; attempt vagal maneuvers; adenosine (if regular); B blocker or calcium channel blocker, if hypotensive can use digoxin; get help if needed!

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.

1) Adenosine can be dangerous! It is a relatively safe medication for confirmed narrow complex tachycardias such as a PSVT. Generally, if a rhythm is wide complex and irregular, avoid adenosine (either the diagnosis is VT and it is ineffective or preexcitation atrial fibrillation which can precipitate ventricular fibrillation).

2) Do not cardiovert sinus tachycardia or multifocal atrial tachycardia, it is not effective.

4) If atrial fibrillation or atrial flutter are diagnosed, determine the duration of the arrhythmia. If > 48 hours or duration is unknown do not chemically or electrically cardiovert without first performing a transesophageal echocardiogram (TEE) as it could precipitate stroke.

5) Is electrical cardioversion a safe option for your patient? (Other comorbidities?)

Synchronized Cardioversion: Initial Recommended Doses

  • Narrow regular: 50-100 J
  • Narrow irregular: 120-200 J biphasic or 200 J monophasic
  • Wide regular: 100 J
  • Wide irregular: defibrillation dose (NOT synchronized)

Adenosine IV Dose:

  • First dose: 6 mg rapid IV push; follow with NS flush (central IV access should provide faster delivery of medication and thus higher doses may not be necessary)
  • Second dose: 12 mg if required

Antiarrhythmic Infusions for Stable Wide-QRS Tachycardia

Either amiodarone and lidocaine is considered recommended therapy in patients with left ventricular dysfunction (EF <40%). Avoid using 2 or more antiarrhythmics together.

Amiodarone IV dose:

  • First dose: 150 mg (or 5 mg/kg) IV bolus over 10 minutes. Repeat as needed (additional boluses of 150 mg over 10 minutes every 10-15 minutes) if VT recurs. Follow by maintenance infusion of 1 mg/min for first 6 hours. The maximum total dose (including doses given during resuscitation) is 2.2 grams in 24 hours.

Lidocaine IV dose:

  • 0.5 to 0.75 mg/kg IV push; repeat every 5 to 10 minutes as needed. May concurrently start a continuous IV infusion of 1 to 4 mg/min. The maximum dose if 3 mg/kg over one hour.

IV. What’s the evidence?

Blomström-Lundqvist, C, Scheinman, M, Aliot, E. “ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias – executive summary: a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias).”. Developed in Collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol.. vol. 42. 2003. pp. 1493-1531.

“ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation).”. J Am Coll Cardiol. vol. 48. 2006. pp. e149

Ganz, LI, Friedman, PL. “Supraventricular tachycardia.”. N Engl J Med 1995;. vol. 332. pp. 162

Neumar, RW, Otto, CW, Link, MS. “Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.”. Circulation. 2010;. vol. 122. pp. S729-S767.