What Is The Main Causes of Tachycardia, Diagnosis

What Is The Main Causes of Tachycardia/Tachycardia conventionally but arbitrarily defined as an atrial and/or ventricular rate of >100 beats per minute, is encountered commonly and can be physiological or pathological in origin. Various adverse consequences from tachycardia have been recognized, and an important one is an association between persistent tachycardia and cardiomyopathy.

Tachycardia also called tachyarrhythmia, is a heart rate that exceeds the normal resting rate.[rx] In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults.[rx] Heart rates above the resting rate may be normal (such as with exercise) or abnormal (such as with electrical problems within the heart). The upper threshold of a normal human resting heart rate is based on age.

Cutoff values for tachycardia in different age groups are fairly well standardized; typical cutoffs are listed below:[rx]

  • 1–2 days – Tachycardia > 159 beats per minute (bpm)
  • 3–6 days – Tachycardia >166 bpm
  • 1–3 weeks – Tachycardia >182 bpm
  • 1–2 months – Tachycardia >179 bpm
  • 3–5 months – Tachycardia >186 bpm
  • 6–11 months – Tachycardia >169 bpm
  • 1–2 years – Tachycardia >151 bpm
  • 3–4 years – Tachycardia >137 bpm
  • 5–7 years – Tachycardia >133 bpm
  • 8–11 years – Tachycardia >130 bpm
  • 12–15 years – Tachycardia >119 bpm
  • >15 years – adult – Tachycardia >100 bpm

Heart rate is considered in the context of the prevailing clinical picture. For example: in sepsis >90 bpm is considered tachycardia.

Types of Tachycardia


  • Atrial fibrillation
  • Atrial flutter
  • Atrial tachycardia
  • AV nodal reentrant tachycardia
  • AV reentrant tachycardia
  • Permanent junctional reciprocating tachycardia (PJRT)


  • Idiopathic ventricular tachycardia
  • Fascicular tachycardia (left septal ventricular tachycardia)


  • Frequent premature ventricular contractions
  • Frequent premature atrial contractions


  • High-rate atrial pacing
  • Persistent rapid ventricular pacing

Atrial tachycardia tends to occur in individuals with structural heart disease, with or without heart failure, and ischemic coronary artery disease. However, focal atrial tachycardia often occurs in healthy individuals without structural heart disease. Other possible etiologies are listed below:

Causes of Tachycardia

Etiological causes

  • Hypoxia
  • Pulmonary disease
  • Ischemic heart disease
  • Stimulants: cocaine, caffeine, chocolate, ephedra
  • Alcohol
  • Metabolic disturbances
  • Digoxin toxicity
  • Heightened sympathetic tone

Some other causes of tachycardia include

  • Adrenergic storm
  • Alcohol
  • Amphetamine
  • Anemia
  • Antiarrhythmic agents
  • Anxiety
  • Atrial fibrillation
  • Atrial flutter
  • Atrial tachycardia
  • AV nodal reentrant tachycardia
  • Brugada syndrome
  • Caffeine
  • Cannabis (drug)
  • The early manifestation of circulatory shock
  • Cocaine
  • Dysautonomia
  • Exercise
  • Fear
  • Fever
  • Hypoglycemia
  • Hypovolemia
  • Hyperthyroidism
  • Hyperventilation
  • Infection
  • Junctional tachycardia
  • Methamphetamine
  • Methylphenidate
  • Multifocal atrial tachycardia
  • Nicotine
  • Pacemaker mediated
  • Pain
  • Pheochromocytoma
  • Sinus tachycardia
  • Supraventricular tachycardia
  • Tricyclic antidepressants
  • Ventricular tachycardia
  • Wolff–Parkinson–White syndrome

Symptoms of Tachycardia

  • Dizziness
  • Lightheadedness
  • Shortness of breath
  • Chest pain
  • Heart palpitations
  • Fainting (syncope)
  • Lightheadedness or dizziness
  • Rapid heartbeat or palpitations
  • Fluttering in the chest
  • Bounding pulse
  • Chest pressure, tightness or pain (angina)
  • Shortness of breath
  • Cardiac arrest
  • Fatigue
  • Unconsciousness

Diagnosis of Tachycardia

EKG can aid the diagnosis of focal atrial tachycardia. EKG features may also inform the origin of focal atrial tachycardias. Electrocardiographic features include:

  • Atrial rate: 100 to 250 BPM
  • Ventricular conduction can be variable
    • Irregular or irregularly irregular in the setting of variable AV block
    • Regular if 1 to 1, 2 to 1, or 4 to 1 AV block
  • P wave morphology
  • Unifocal, but similar in morphology to each other
  • Might be inverted
  • Differs from normal sinus P wave
  • May exhibit either long RP or short PR intervals
  • Rhythm may be paroxysmal or sustained
    • May demonstrate an increase in the rate at initiation (i.e., “warm-up,” or “rev up”)
    • May demonstrate a decrease in the rate at termination (i.e., “cool down”)

Below is a differential of similar appearing arrhythmias with their identifying features.

Narrow complex, regular tachycardias

Sinus tachycardia

  • P wave with superior axis

Atrial flutter

  • Biphasic, sawtooth appearing F wave
  • Difficult to identify isoelectric, baseline PR segment

Typical atrial flutter

  • Involves circuit around the tricuspid annulus
  • Counterclockwise flutter produces F waves that are negative in lead II and positive in lead V1
  • Clockwise flutter produces F waves that are positive in lead II and negative in lead V1

Atypical atrial flutter

  • Involves circuit around the scar, left atrium, otherwise non-cavotricuspid isthmus dependent


Typical, slow-fast AVNRT

  • Short RP interval
  • P wave may be absent or within the S wave

Atypical, fast-slow AVNRT

  • Long RP interval
  • P wave negative before QRS


  • Baseline EKG may demonstrate pre-excitation
  • Antidromic (propagation proceeds through the accessory pathway, and then retrogradely through the Purkinje system, to His bundle, through the AV node and back through accessory pathway)
    • QRS width: Wide
    • RP interval: Short
  • P wave, PR interval, QRS are variable depending on accessory pathway location and conduction direction
  • Orthodromic (propagation proceeds down AV node, His bundle, Purkinje fibers, retrograde through accessory pathway and back to AV node)
  • QRS width: Narrow
  • RP interval: Long
  • Atrial tachycardia (Focal)
  • Junctional tachycardia
    • P wave may be absent or inverted
    • If retrograde VA conduction, inverted P wave may occur just before or after the QRS complex

Narrow complex, irregular tachycardia

  • Atrial fibrillation
  • Irregularly irregular rhythm
  • Atrial flutter, atrial tachycardia with variable AV block
    • Has features of atrial flutter or atrial tachycardia, although variable block leads to irregular rhythm
  •  Multifocal atrial tachycardia
    • P wave morphology with greater than or equal to 3 distinct morphologies
  •  Resting ECG
  • Holter monitoring, as arrhythmias develop when heart rate increases
  • Exercise stress test both for diagnosis and monitoring of therapy
  • Echocardiogram and/or MRI to evaluate for structural defects
  • Consultation with a clinical geneticist and/or genetic counselor

Suggestive Findings

Catecholaminergic polymorphic ventricular tachycardia (CPVT) should be suspected in individuals who have one or more of the following []:

  • Syncope occurring during physical activity or acute emotion; mean onset age seven to 12 years. Less frequently, first manifestations may occur later in life; individuals with the first event up to age 40 years are reported.
  • History of exercise- or emotion-related palpitations and dizziness in some individuals
  • Sudden unexpected cardiac death triggered by acute emotional stress or exercise
  • Family history of juvenile sudden cardiac death triggered by exercise or acute emotion
Exercise-induced polymorphic ventricular arrhythmias
  • ECG during a graded exercise (exercise stress test)* allows ventricular arrhythmias to be reproducibly elicited in the majority of affected individuals. Typically, the onset of ventricular arrhythmias is 100-120 beats/min.
  • With an increase in workload, the complexity of arrhythmias progressively increases from isolated premature beats to bigeminy and runs of non-sustained ventricular tachycardia (VT). If the affected individual continues exercising, the duration of the runs of VT progressively increases and VT may become sustained.
  • An alternating 180°-QRS axis on a beat-to-beat basis, so-called bidirectional VT, is often the distinguishing presentation of CPVT arrhythmias.
  • Some individuals with CPVT may also present with irregular polymorphic VT without a “stable” QRS vector alternans [].
  • Exercise-induced supraventricular arrhythmias (supraventricular tachycardia and atrial fibrillation) are common [].
  • Ventricular fibrillation occurring in the setting of acute stress
  • Absence of structural cardiac abnormalities

Establishing the Diagnosis

According to the most recent version of the International Guidelines on sudden cardiac death [], the diagnosis of CPVT is established

  • In the presence of a structurally normal heart, normal resting ECG, and exercise- or emotion-induced bidirectional or polymorphic ventricular tachycardia;
  • In individuals who have a heterozygous pathogenic variant in RYR2 or CALM1 or biallelic pathogenic variants in CASQ2 or TRDN [rx].
  • Molecular testing approaches can include serial single-gene testing, use of a multigene panel, and more comprehensive genomic testing
Serial single-gene testing
  • Sequence analysis of RYR2 can be performed first and followed by sequence analysis of CASQ2 if no pathogenic variant is found. If no pathogenic variant in CASQ2 is found, sequence analysis of CALM1and TRDN should be performed next, keeping in mind that pathogenic variants in CALM1 and TRDN are extremely rare causes of CPVT.
  • Gene-targeted deletion/duplication analysis of RYR2 can be performed next if a pathogenic variant in RYR2 or CALM1 or biallelic pathogenic variants in CASQ2 or TRDN have not been identified [rx].
A multigene panel that includes CALM1CASQ2RYR2, and TRDN and other genes of interest (see Differential Diagnosis) may also be considered. Note:
  • The genes included in the panel and the diagnostic sensitivity of the testing used for each gene vary by laboratory and are likely to change over time.
  • Some multigene panels may include genes not associated with the condition discussed in this GeneReview; thus, clinicians need to determine which multigene panel is most likely to identify the genetic cause of the condition at the most reasonable cost while limiting identification of variants of uncertain significance and pathogenic variants in genes that do not explain the underlying phenotype.
  • In some laboratories, panel options may include a custom laboratory-designed panel and/or custom phenotype-focused exome analysis that includes genes specified by the clinician.
  • Methods used in a panel may include sequence analysis, deletion/duplication analysis, and/or other non-sequencing-based tests.
    For an introduction to multigene panels click here. More detailed information for clinicians ordering genetic tests can be found here.
More comprehensive genomic testing – (when available) including exome sequencing and genome sequencing may be considered if serial single-gene testing (and/or use of a multigene panel that includes CALM1CASQ2RYR2, and TRDN) fails to confirm a diagnosis in an individual with features of CPVT. Such testing may provide or suggest a diagnosis not previously considered (e.g., mutation of a different gene or genes that results in a similar clinical presentation).
  • Magnetic resonance imaging (MRI) A cardiac MRI can provide still or moving pictures of how the blood is flowing through the heart and detect irregularities.
  • Computerized tomography (CT)CT scans combine several X-ray images to provide a more detailed cross-sectional view of the heart.
  • Coronary angiogram –  To study the flow of blood through your heart and blood vessels, your doctor may use a coronary angiogram to reveal potential blockages or abnormalities. It uses a dye and special X-rays to show the inside of your coronary arteries.
  • Chest X-ray – This test is used to take still pictures of your heart and lungs and can detect if your heart is enlarged.

Stress Test

  • Your doctor may recommend a stress test to see how your heart functions while it is working hard during exercise or when medication is given to make it beat fast. In an exercise stress test, electrodes are placed on your chest to monitor heart function while you exercise, usually by walking on a treadmill. Other heart tests may also be performed in conjunction with a stress test.

Additional Tests

  • Your doctor may order additional tests as needed to diagnose an underlying condition that is contributing to tachycardia and judge the condition of your heart.

Event Recorder

This device is similar to a Holter monitor, but it does not record all the heartbeats. There are two types:

  • One type uses a phone to transmit signals from the recorder while the person is experiencing symptoms.
  • The other type is worn all the time for a long time. These can sometimes be worn for as long as a month.

This event recorder is good for diagnosing rhythm disturbances that happen at random moments.

Electrophysiological Testing (EP studies)

  • This is an invasive, relatively painless, non-surgical test and can help determine the type of arrhythmia, its origin, and potential response to treatment. The test is carried out in an EP lab by an electrophysiologist and makes it possible to reproduce troubling arrhythmias in a controlled setting.

Tilt-Table Test

  • If an individual experiences fainting spells, dizziness, or lightheadedness, and neither the ECG nor the Holter revealed any arrhythmias, a tilt-table test might be performed. This monitors blood pressure, heart rhythm, and heart rate while they are moved from a lying to an upright position. When reflexes work correctly, they cause the heart rate and blood pressure to change when moved to an upright position. This is to make sure the brain gets an adequate supply of blood.

Treatment of Tachycardia

But if the episodes are prolonged, or recur often, your doctor may recommend treatment, including

  • Carotid sinus massage – A healthcare professional can apply gentle pressure on the neck, where the carotid artery splits into two branches.
  • Pressing gently on the eyeballs with eyes closed. Caution – This procedure should be supervised carefully by a healthcare physician.
  • Valsalva maneuver – This consists of holding your nostrils closed while blowing air through your nose.
  • Using the dive reflex – The dive reflex is the body’s response to sudden immersion in water, especially cold water.
  • Sedation
  • Cutting down on coffee or caffeinated substances
  • Cutting down on alcohol
  • Quitting tobacco use
  • Getting more rest

Pharmacologic Treatment

  • If vagal maneuvers fail – a trial of intravenous adenosine may be given at an initial dose of 6 mg and a subsequent dose of 12 mg., Its use may serve as a diagnostic and therapeutic tool because it will terminate almost all AVNRTs and AVRTs by breaking the AV-nodal dependent circuit. In patients with non–AV-nodal dependent circuits (i.e., focal atrial tachycardia and atrial flutter), intravenous use of adenosine may prove to be a valuable diagnostic tool because the transient AV block may unmask ectopic atrial P waves or flutter waves. Patients should always be monitored by ECG during adenosine administration.
  • Adenosine – may induce a wide range of transient bradycardias (including sinus arrest and asystole) as well as atrial fibrillation, SVT and ventricular tachycardia. Albeit very rare, cases of sustained ventricular tachycardia, ventricular fibrillation, and Torsades de pointes have been reported. In patients with underlying coronary disease, adenosine may lead to coronary steal syndrome and subsequent myocardial ischemia.  Adenosine should therefore always be administered with an external pacemaker or defibrillator nearby.
  • When vagal maneuvers and adenosine – fail to terminate a narrow-complex tachycardia, intravenous treatment with a nondihydropiridine calcium-channel blocker (e.g., diltiazem and verapamil) or β-blocker may be used. Calcium-channel blockers terminate 64%–98% of SVTs in hemodynamically stable patients. Administering a calcium-channel blocker intravenously over 20 minutes has been shown to reduce the rate of hypotension. There are fewer data supporting the use of β-blockers in the acute treatment of SVT; however, they are considered reasonable choices because of their safety profile.,
  • If all aforementioned pharmacologic therapies fail – synchronized cardioversion is recommended, even in hemodynamically stable patients.
  • In patients presenting in atrial fibrillation who have known Wolff–Parkinson – White or new pre-excitation pattern on ECG, the use of potent AV-nodal blockers (i.e., β-blockers, diltiazem, verapamil, and digoxin) should be avoided because these medications may potentiate conduction over the accessory pathway and lead to potentially life-threatening ventricular arrhythmias. In these cases, intravenous use of procainamide is the preferred approach in the acute setting.
  • Adenosine is rapidly metabolized in the periphery – and therefore must be given as a rapid push through a large, ideally peripheral, intravenous route. The initial dose is 6 mg intravenously (IV) (pediatric dose 0.1 mg/kg, maximum dose of 6 mg). If the initial dose is ineffective, adenosine may be dosed again at 12 mg IVP (pediatric dose 0.2 mg/kg, maximum dose 12 mg). The second dose of adenosine 12 mg IVP may be repeated one additional time if there is no effect. Each dose of adenosine needs to be flushed rapidly with 10 mL to 20 mL normal saline. Often two-person administration, with one person administering the adenosine at a proximal IV port, and a second person flushing the IV line via a distal port immediately after adenosine administration, is required to adequate flush in the adenosine.
  • Consider reducing the adenosine dose to 3 mg – IVP if the patient is currently receiving carbamazepine or dipyridamole, is the recipient of a heart transplant, or adenosine is being given through a central line.
  • If adenosine fails – second line medications include diltiazem (0.25 mg/kg IV loading dose followed by 5mg/hr to 15 mg/hr infusion), esmolol (0.5 mg/kg IV loading dose, then 0.5 mg/kg/min up to 0.2 mg/kg/min, will need to repeat bolus for every up-titration), or metoprolol (2.5 mg to 5 mg IV every two to five minutes, not to exceed 15 mg over 10 to 15 minutes).

Summary of recommendations from the 2015 guideline of the American College of Cardiology, the American Heart Association and the Heart Rhythm Society on the management of adults with supraventricular tachycardia (SVT) [

Acute treatment

  • Vagal maneuvers are recommended for acute treatment in patients with regular SVT (class I recommendation, level B-R evidence)
  • Intravenous administration of adenosine is recommended for acute treatment in patients with regular SVT (class I recommendation, level B-R evidence)
  • Synchronized cardioversion is recommended for acute treatment in patients with hemodynamically stable SVT when pharmacologic treatment is ineffective or contraindicated (class I recommendation, level B-NR evidence)
  • Intravenous administration of diltiazem or verapamil can be effective for acute treatment in patients with hemodynamically stable SVT (class IIa recommendation, level B-R evidence)
  • Intravenous use of β-blockers is reasonable for acute treatment in patients with hemodynamically stable SVT (class IIa recommendation, level C-LD evidence)

Ongoing management

  • Oral β-blocker – diltiazem or verapamil treatment is useful for ongoing management in patients with symptomatic SVT who do not have ventricular pre-excitation during sinus rhythm (class I recommendation, level B-R evidence)
  • Electrophysiologic study – with the option of radiofrequency catheter ablation is useful for the diagnosis and potential treatment of SVT (class I recommendation, level B-NR evidence)
  • Patients with SVT – should be educated on how to perform vagal maneuvers for ongoing management of SVT (class I recommendation, level C-LD evidence)

Referral for radiofrequency catheter ablation

  • Catheter ablation of the slow pathway is recommended in patients with AVNRT (class I recommendation, level B-NR evidence)
  • Catheter ablation is recommended in patients with symptomatic focal atrial tachycardia as an alternative to pharmacologic treatment (class I recommendation, level B-NR evidence)
  • Catheter ablation of the accessory pathway is recommended in patients with AVRT or pre-excited atrial fibrillation (class I recommendation, level B-NR evidence)
  • An electrophysiologic study is reasonable in asymptomatic patients with pre-excitation to stratify risk for arrhythmic events (class IIa recommendation, level B-NR evidence)
  • Catheter ablation of the cavotricuspid isthmus is useful in patients with atrial flutter that is either symptomatic or refractory to pharmacologic rate control (class I recommendation, level B-R evidence)

Note: AVNRT = atrioventricular nodal re-entrant tachycardia, AVRT = atrioventricular re-entrant tachycardia.

  • Class I = strong recommendation where benefits > risks; class IIa = moderate-strength recommendation where benefits >> risks.
  • Level B-R = moderate-quality evidence from one or more randomized controlled trials (RCTs) or meta-analyses of moderate-quality RCTs;
  • Level B-NR = moderate-quality evidence from one or more nonrandomized or observational or registry studies;
  • Level C-LD = limited data from RCTs or nonrandomized observational or registry studies with limitations of design or execution.


Complications are either related to the medications or radiofrequency ablation. Since the latter is an invasive procedure the following complications may occur:

  • Hematoma
  • Pseudoaneurysm of the artery
  • Bleeding
  • Myocardial infarction
  • Heart block and the need for a pacemaker
  • Stroke
  • Death
  • Overall, focal atrial tachycardia is a benign arrhythmia.
  • Focal atrial tachycardia typically occurs secondary to an underlying disease process or acute illness.
  • Focal atrial tachycardia is one form of atrial tachycardia. Atrial activation patterns in focal atrial tachycardia will be similar during the tachycardia, yet distinct from the normal sinus P wave. Focal atrial tachycardia can be regular or irregular if variable block exists. A “warm-up” and “cool down” pattern can occur during initiation and termination, respectively.
  • Patients can be asymptomatic or present with palpitations, chest pain, lightheadedness, dizziness, or presyncope. Focal atrial tachycardia often presents on telemetry on asymptomatic or sleeping patients.
  • Ventricular rate control is achievable with calcium channel or beta-blockers. If the patient remains persistently tachycardic or has uncontrolled symptoms, the patient may benefit from antiarrhythmic therapy with class IC or III antiarrhythmics.
  • A possible significant cardiac sequella of prolonged atrial tachycardia (or any tachycardia) is tachycardia-induced cardiomyopathy. If there are concerns for high tachycardia burden, outpatient monitoring may be necessary.


The most effective way to prevent tachycardia is to maintain a healthy heart and reduce your risk of developing heart disease. If you already have heart disease, monitor it and follow your treatment plan to lower your tachycardia risk.

Prevent Heart Disease

Treat or eliminate risk factors that may lead to heart disease. Take the following steps:

  • Exercise and eat a healthy diet – Live a heart-healthy lifestyle by exercising regularly and eating a healthy, low-fat diet that’s rich in fruits, vegetables, and whole grains.
  • Maintain a healthy weight – Being overweight increases your risk of developing heart disease.
  • Keep blood pressure and cholesterol levels under control – Make lifestyle changes and take medications as prescribed to correct high blood pressure (hypertension) or high cholesterol.
  • Stop smoking – If you smoke and can’t quit on your own, talk to your doctor about strategies or programs to help you break a smoking habit.
  • Drink in moderation – If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women of all ages and men older than age 65, and up to two drinks a day for men age 65 and younger. For some conditions, it’s recommended that you completely avoid alcohol. Ask your doctor for advice specific to your condition.
  • Don’t use recreational drugs – Don’t use stimulants, such as cocaine. Talk to your doctor about an appropriate program for you if you need help ending recreational drug use.
  • Use over-the-counter medications with caution – Some cold and cough medications contain stimulants that may trigger a rapid heartbeat. Ask your doctor which medications you need to avoid.
  • Limit caffeine – If you drink caffeinated beverages, do so in moderation (no more than one to two beverages daily).
  • Control stress – Avoid unnecessary stress and learn coping techniques to handle normal stress in a healthy way.
  • Go to scheduled checkups – Have regular physical exams and report any signs or symptoms to your doctor.

Monitor and treat existing heart disease

If you already have heart disease, you can take steps to lower your risk of developing tachycardia or another arrhythmia:

  • Follow the plan – Be sure you understand your treatment plan and take all medications as prescribed.
  • Report changes immediately – If your symptoms change or get worse or you develop new symptoms, tell your doctor immediately.


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What Is The Main Causes of Tachycardia

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