Etiology

The etiology of tachycardia is variable and often multifactorial. The most common type is sinus tachycardia. Cases of tachyarrhythmias not due to a heightened sinus rate may be due to focal islets of tissue that fire rapidly because of increased automaticity, triggered activity, or reentry within a tissue with heterogeneous conduction properties. Secondary causes of tachyarrhythmia include ion channelopathies, myocardial scar, surgical scar, increased atrial or ventricular wall tension and stretch due to elevated filling pressures, ischemia, electrolyte abnormalities, increased intrinsic catecholamines, myocarditis, or any combination of these causes. Prescribed, legitimate, and illicit drug use have been implicated.

Narrow QRS (duration <120 ms) with a regular ventricular rhythm

Sinus tachycardia

A rhythm that originates in the sinoatrial (sinus) node with a rate above 100 bpm. This is usually a normal response to physical, emotional, physiologic, or pharmacologic stress. Secondary causes of sinus tachycardia include physical deconditioning, hypoxia, pulmonary embolism, hypovolemia, hyperthyroidism, anemia, drugs (e.g., caffeine, alcohol, nicotine, amphetamines, cocaine), and prescribed medications (e.g., aminophylline, atropine, clozapine, catecholamines).[1][2][19]

Postural orthostatic tachycardia syndrome (POTS)

A chronic, multisystem disorder that is thought to be due to an autoimmune process. POTS is characterized by:[20][21][22][23]​​​​​​

  • frequent symptoms of orthostatic intolerance (that improve rapidly when the patient returns to a supine position) that interfere with daily living activities, and have continued for at least 3 months, and

  • an increase in heart rate by ≥30 bpm (or ≥40 bpm in patients ages 12 to 19 years) within 10 minutes of standing from a supine position or head-up tilt (without orthostatic hypotension) that is not due to other causes of sinus tachycardia.

Inappropriate sinus tachycardia

A persistent increase in resting heart rate unrelated to or out of proportion to physical, emotional, pathologic, or pharmacologic stress (resting heart rate >100 bpm or average heart rate >90 bpm in 24-hour ECG monitoring). The precise etiology is unknown and is likely to be multifactorial. Increased sinus node automaticity and autonomic dysfunction have been proposed as possible causes.[1][2][21]

Atrial tachycardia

Rapid atrial activation from a region of the atria other than the sinus node with rates typically between 100 and 250 bpm. Multifocal atrial tachycardia is defined as three or more sites of atrial activation (commonly irregular rhythm). Focal atrial tachycardia can occur without cardiac disease. Atrial tachycardia with AV block should raise the suspicion for digitalis toxicity. Hypokalemia can also exacerbate this condition.[24] Right-sided atrial tachycardias tend to originate from the crista terminalis, tricuspid annulus, or coronary sinus ostium. Left-sided atrial tachycardias often originate from around the pulmonary veins, atrial septum, or mitral annulus.[1][2]

Atrial flutter

Organized reentrant rhythm with atrial rates typically 250 to 350 bpm and ventricular rates often 145 to 150 bpm (due to 2:1 block) involving large areas of the atrium. In typical atrial flutter, the macroentry atrial circuit rotates around the tricuspid valve and between the inferior vena cava and tricuspid annulus. This essential part of the circuit can be a target for catheter ablation.[1][2][Figure caption and citation for the preceding image starts]: Atrial flutterFrom the collection of Robert W. Rho, MD; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@467e7774[Figure caption and citation for the preceding image starts]: Atrial flutter (detail)From the collection of Robert W. Rho, MD; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@2c50125f

Sinus node reentry tachycardia

A tachycardia that originates from reentry circuits that involve the sinus node and perinodal tissue. It is presumed to be secondary to heterogeneous conduction properties of the sinus node and perinodal tissue.[1][2]

AV nodal reentrant tachycardia (AVNRT)

A reentrant tachycardia involving two pathways within the AV node or perinodal atrial tissue. One pathway has rapid conduction and a relatively long refractory period; the second pathway has slow conduction and a shorter refractory period. Following a premature atrial impulse, the fast pathway is still refractory from the previous impulse but anterograde conduction can occur through the slow pathway, which is no longer refractory. By the time slow-pathway conduction is complete, the fast pathway is no longer refractory and retrograde conduction can occur. If the slow pathway is no longer refractory following retrograde conduction, the cycle repeats. A less common form of AVNRT ("atypical" AVNRT) involves anterograde conduction down the fast pathway, resulting in a reentry circuit that turns in the opposite direction to the more common "typical" AVNRT described above.[1][2]

AV reciprocating tachycardia (AVRT)

A reentrant tachycardia circuit that involves an accessory pathway as well as the native AV node. The most common form (approximately 90% of cases) is orthodromic AVRT.[25]​ The arrhythmia results from anterograde conduction through the AV node and retrograde conduction through the accessory pathway. This results in a narrow-complex tachycardia because the ventricle is activated anterograde through the His-Purkinje system.[26]

Permanent junctional reciprocating tachycardia

A form of orthodromic AVRT involving anterograde conduction through the AV node and retrograde accessory-pathway conduction. The retrograde limb of this reentry circuit is characterized by slow conduction, creating a very stable circuit (anterograde down the AV node and retrograde up the slowly conducting bypass tract). The descriptive term "permanent" is added to reflect its stable nature and tendency to recur frequently and dominate sinus rhythm. For this reason, this arrhythmia can sometimes cause a tachycardia-mediated cardiomyopathy. This rhythm has rates between 120 and 200 bpm.[1][2] It is most commonly seen in infants and children.[1][2]

Junctional ectopic tachycardia

This rhythm is caused by abnormal rapid discharges from the junctional region (distal AV node or proximal His-Purkinje system) and does not require atrial or ventricular involvement to originate. The congenital form is insidious in presentation and is often identified in infants only after the development of tachycardia-induced cardiomyopathy. It is sometimes seen after cardiac surgery and may result in hemodynamic instability because of its rate and lack of AV synchrony. Clinical factors that may predispose to this arrhythmia include digitalis toxicity, hypokalemia, myocardial ischemia, cardiac surgery, and inflammatory myocarditis.[1][2]

Narrow QRS (duration <120 ms) with an irregular ventricular rhythm

Atrial fibrillation

A supraventricular tachyarrhythmia characterized by an irregularly irregular rhythm due to the rapid and random conduction of irregular impulses to the ventricle. The irregular impulses are due to multiple wavelets of reentry that rotate randomly within the atria and randomly bombard the AV node.[27]​ Risk of atrial fibrillation is increased in patients treated for hypertriglyceridemia with medication containing omega-3-acid ethyl esters, particularly at high doses.[28][29][30]

Atrial tachycardia or flutter with variable AV conduction

In contrast to atrial fibrillation, rapid atrial tachycardia and atrial flutter result in fast but regular impulses to the AV node. Conduction of impulses to the ventricle is variable but tends to be "regularly irregular" and with a pattern.[1][2]

Multifocal atrial tachycardia

This arrhythmia involves at least three distinct competing atrial foci. Multifocal atrial tachycardia is most often associated with pulmonary disease but has also been associated with cardiac disease (valvular, hypertensive, coronary) as well as a variety of other systemic conditions, including hypokalemia, hypomagnesemia, and sepsis, and certain medications (including isoproterenol and aminophylline).[31][32]

Wide QRS (duration >120 ms) with a regular ventricular rhythm

Atrial tachycardia, atrial flutter, and common supraventricular tachycardias that conduct with aberrancy to the ventricle (left bundle branch block or right bundle branch block) are an important part of the differential diagnosis of etiologies of wide-complex tachycardias with uniform QRS duration and morphology.

Idiopathic ventricular tachycardia (VT) (monomorphic VT associated with a structurally normal heart)

Repetitive monomorphic ventricular tachycardia: a focal arrhythmia that is thought to be due to triggered activity. Typically, it originates from the right ventricular outflow tract (when it is known as right ventricular outflow tract tachycardia). The etiology is unknown. It is mostly seen in young and middle-aged patients of both sexes with a structurally normal heart and is often provoked by exercise, emotion, stress, or hormone fluctuations.[33] Less commonly the site of origin may be in the LV outflow tract, the LV epicardium, above the pulmonary valve, or along the septal aspect of the mitral annulus. VT that maps to these regions behaves similarly to “right ventricular outflow tract VT” and typically follows a benign clinical course.

Idiopathic left VT: occurs due to reentry around the specialized conduction tissue and slow calcium-ion-sensitive myocardial tissue. The etiology of this arrhythmia is unknown. It is sensitive to calcium channel blockers, which may terminate and control the arrhythmia. The reentry circuit usually involves the left posterior fascicle and the VT is therefore relatively narrow, with a right bundle branch block and a superior axis on the 12-lead ECG. It is seen in patients aged 15 to 40 years with structurally normal hearts. Seventy percent of cases are in males. In most cases, this VT is not associated with an increased risk of sudden death.[34][35]

Accelerated idioventricular rhythm

An automatic focus originating in the ventricular myocardium. Similar to VT, though rates are no more than 20% faster than the sinus rate (typically 80-120 bpm).[34]

Monomorphic VT associated with prior myocardial infarction

An arrhythmia that usually originates at the interface between healthy and damaged myocardium and is most commonly a reentrant rhythm.[36] It is more commonly seen with larger infarctions and in patients with a depressed ejection fraction.

Monomorphic VT associated with nonischemic cardiomyopathy

Regardless of the etiology of the cardiomyopathy, heterogeneous conduction properties within the ventricular myocardium due to cardiomyopathy can serve as a substrate for reentry and result clinically in VT. Some specific cardiomyopathies merit special attention.[34]

  • Arrhythmogenic right ventricular dysplasia: characterized by fatty right ventricular infiltration and fibrosis or thinning. VT is due to reentry within this complicated substrate.

  • Bundle branch reentry VT: a common cause of sustained VT in patients with nonischemic dilated cardiomyopathy. The reentry circuit usually conducts anterograde down the right bundle branch, across the ventricular septum, and conducts retrograde up the left bundle branch. The characteristic 12-lead ECG shows a left bundle branch block pattern during VT because of this pattern of activation.

  • Cardiac sarcoidosis: may present with arrhythmias (such as advanced AV block or VT) and/or unexplained new onset heart failure without a history of systemic sarcoidosis.[37]​​[38][39]​​​ The patchy formation of granulomas, fibrosis, and scarring leads to VT due to reentry within this complicated substrate.[37]​​ Clinically overt cardiac sarcoidosis has been reported in 5% to 10% of cases with systemic sarcoidosis.[37][40][41]​ Cardiac sarcoidosis has been confirmed in approximately one third of middle-aged patients (37%) presenting with unexplained high-grade atrioventricular block.[42]

  • Chagas cardiomyopathy: VT is predominantly seen in chronic Chagas cardiomyopathy, which is probably caused by an autoimmune response to infection with Trypanosoma cruzi. The mechanism is likely to be related to the resulting fibrosis of the myocardium. The mechanism of VT is reentry within this complicated substrate.

Rapid atrial arrhythmias associated with a "bystander" accessory pathway

Any atrial arrhythmia (atrial flutter, supraventricular tachycardia ) that normally conducts through the native His-Purkinje system and would manifest with a narrow QRS can instead present as a wide-complex tachycardia if there is also an associated accessory pathway.[1][2] Additionally, with rapid supraventricular rhythms, a rate-related bundle branch may develop only at times of tachycardia, resulting in a wide-complex-tachycardia morphology.

Antidromic AV reciprocating tachycardia

Reentrant circuit in which an anterograde circuit conducts down the accessory pathway and retrograde back up the AV node, resulting in a wide-QRS-complex morphology. The reentry circuit in this arrhythmia is the same as that in orthodromic AV reciprocating tachycardia but in the opposite direction. Because activation is anterograde down the accessory pathway, the QRS complex is maximally preexcited during tachycardia.[1][2]

Paced rhythm

Patients with pacemakers can present with wide-complex tachycardia secondary to rapid ventricular pacing. Most commonly this is due to a dual chamber device tracking an atrial arrhythmia (atrial tachycardia and atrial flutter) with subsequent rapid ventricular pacing. [Figure caption and citation for the preceding image starts]: Right ventricular outflow tract ventricular tachycardiaFrom the collection of Robert W. Rho, MD; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@116ed456[Figure caption and citation for the preceding image starts]: Ventricular tachycardia in a patient with arrhythmogenic right ventricular cardiomyopathyFrom the collection of Robert W. Rho, MD; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@f9e7981[Figure caption and citation for the preceding image starts]: Supraventricular tachycardia with aberrancy and left bundle branch blockFrom the collection of Robert W. Rho, MD; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@47a57c17[Figure caption and citation for the preceding image starts]: Rate-related left bundle branch blockFrom the collection of Robert W. Rho, MD; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@78f13a2b[Figure caption and citation for the preceding image starts]: Antidromic reentrant tachycardiaFrom the collection of Robert W. Rho, MD; used with permission [Citation ends].com.bmj.content.model.assessment.Caption@24683edf

Wide QRS (duration >120 ms) with an irregular ventricular rhythm

Causes include the following:

  • Atrial fibrillation with a bundle branch block

  • Multifocal atrial tachycardia with a bundle branch block

  • Atrial tachycardia or flutter with variable AV conduction with a bundle branch block or accessory pathway.

Variable QRS duration with an irregular ventricular rhythm

Polymorphic VT with a normal QT interval

Most commonly seen in the context of acute coronary syndrome or myocardial ischemia but can also be seen in structurally normal hearts. In the context of myocardial infarction, the development of polymorphic VT is suggestive of ongoing ischemia; treatment is focused at the underlying ischemia. Ion channelopathies can present with polymorphic VT. Catecholaminergic polymorphic VT occurs in the absence of structural heart disease and often presents as stress- or exercise-induced syncope, or sudden death in childhood or adolescence. A variety of genetic causes have been identified, one of which involves an autosomal dominant mutation in the gene for the cardiac ryanodine receptor.[43] Less commonly, an autosomal recessive mutation in the cardiac calsequestrin gene (CASQ2) has been associated with this condition. Both of these gene mutations are associated with the release of calcium from the sarcoplasmic reticulum.[44]

Torsades de pointes

Polymorphic VT associated with a prolonged QT (observed during sinus rhythm) with a characteristic "twisting on axis" morphology. The prolonged QT may be congenital or acquired. Acquired long-QT syndrome is more commonly observed clinically. It may be secondary to medications known to prolong the QT interval, AZCERT: QT drugs list Opens in new window ischemia, significant electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), or massive injury to the central nervous system.[43][45]​​

Bidirectional VT

A rare but potentially fatal arrhythmia most often caused by digitalis toxicity but also seen in catecholaminergic polymorphic VT and Andersen-Tawil syndrome (long QT 7). It is characterized by two alternating QRS morphologies (often a right bundle branch block with alternating left and right axis). Contrary to ventricular bigeminy, the R-R interval in bidirectional VT is regular.[34]

Atrial fibrillation with ventricular preexcitation

Patients with atrial fibrillation and an anterograde-conducting accessory pathway may present with a wide-complex irregular tachycardia. Some patients may have anterograde conduction pathways with more rapid properties than others and are therefore at greater risk of this arrhythmia. Identification of this arrhythmia is vital because it can lead to ventricular fibrillation and hemodynamic collapse. Preexcited atrial fibrillation is a potentially life-threatening arrhythmia.​[5]

Ventricular fibrillation

Rapid (rate >300 bpm), grossly irregular, life-threatening ventricular rhythm characterized by variable QRS cycle length, morphology, and amplitude.[34]

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