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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammed Salih, MD.


Parasystole is a type of arrhythmia caused by the presence and function of a secondary pacemaker in the heart, which works in parallel with the SA node. Parasystolic pacemakers are protected from depolarization by the SA node by some form of entrance block. This block can be complete or incomplete.

Parasystolic pacemakers can exist in the atrium or the ventriculus. Atrial parasystolia are characterized by being a type of narrow QRS complexes Arrhythmia.

Historical Perspective

  • Parasystole was first reported by Schamroth in 1967.
  • Parasystole as an entity was studied by Kaufmann and Bothberger, but their studies are now interpreted differently.


  • Parasystole may be classified according to location of their origin but in literature no such classification mentioned.
  • Parasystole consists of stimultaneous activity of two (rarely more) independent impulse-forming centers, one of which is "protected" from the other, each competing to activate the atria or ventricles or both.
  • The parasystolic pacemaker may be located anywhere in the heart but is commonly located in the ventricles, less commonly in the A-V node and rarely in the atria.


  • Parasystole is a result of interaction between two fixed rate pacemakers having different discharge rates.
  • Parasystolic pacemakers can exist in either the atrium or the ventricle.
  • The latent pacemaker is protected from being overdriven by the dominant rhythm (usually NSR) by intermittent or constant entrance block (impulses of sinus origin fail to depolarize the latent pacemaker secondary to block in the tissue surrounding the latent pacemaker focus).
  • The depolarized level of membrane potential at which abnormal automaticity occurs can cause entrance block, leading to parasystole. This would be an example of an arrhythmia caused by a combination of an abnormality of impulse conduction and impulse initiation.
  • Such block must be unidirectional, so that activity from the ectopic pacemaker can exit and produce depolarization whenever the surrounding myocardium is excitable.
  • The protected pacemaker is said to be a parasystolic focus. In general, under these conditions, a protected focus of automaticity of this type fires at its own intrinsic frequency, and the intervals between the discharges of each pacemaker are multiples of its intrinsic discharge rate (sometimes described as fixed parasystole).
  • Therefore on the surface electrocardiogram (ECG) the coupling intervals of the manifest ectopic beats wander through the basic cycle of the sinus rhythm.
  • The traditional ECG criteria used to recognize the fixed form of parasystole include:
    • The presence of variable coupling intervals of the manifest ectopic beats.
    • Interectopic intervals that are simple multiples of a common denominat.
    • The presence of fusion beats.
  • The parasystolic focus can exhibit exit block, during which it may fail to depolarize excitable myocardium.
  • The parasystolic focus is protected, it may not be totally immune to the surrounding electrical activity.
  • The effective electrical communication that permits the emergence of the ectopic discharges can also allow the rhythmic activity of the surrounding tissues to electrotonically influence the periodicity of the pacemaker discharge rate.
  • Electrotonic influences arriving during the early stage of diastolic depolarization result in a delay in the firing of the parasystolic focus, whereas those arriving late accelerate the discharge of the parasystolic focus.
  • As a consequence, the dominant pacemaker can entrain the partially protected parasystolic focus and force it to discharge at periods that may be faster or slower than its own intrinsic cycle and give rise to premature discharges whose patterns depend on the degree of modulation and the basic heart rate, occasionally mimic reentry, and occur at fixed coupling intervals.
  • All these features of abnormal automaticity can be found in the Purkinje fibers that survive in regions of transmural MI and cause ventricular arrhythmias during the subacute phase..

Clinical Features

  • Parasystole may feel that heart is racing or beating too slowly.
  • Heart may not pump effectively due to the fast or slow heartbeat.
  • These include shortness of breath, weakness, dizziness, lightheadedness, fainting or near fainting, and chest pain or discomfort.

Differentiating [disease name] from other Diseases

The differentiating features are largely based on both EKG findings and cardiovascular examination.

Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)[1][2]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter[3]
  • Regular or Irregular
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Sawtooth pattern of P waves at 250 to 350 bpm
  • Biphasic deflection in V1
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Atrioventricular nodal reentry tachycardia (AVNRT)[4][5][6][7]
  • Regular
  • 140-280 bpm
  • Slow-Fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R' in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)
  • Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • QRS alternans may be present
Multifocal Atrial Tachycardia[8][9]
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Varying morphology from at least three different foci
  • Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)[10][11]
  • Regular except when disturbed by premature beat(s)
  • 80-120 bpm
  • Upright
  • > 0.12 second
  • May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node
  • Ashman’s Phenomenon:
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[12][13]
  • Regular
  • Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm
  • Less than 0.12 seconds
  • A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
  • A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
Ventricular Fibrillation (VF)[14][15][16]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[17][18]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent

  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI

Epidemiology and Demographics

  • The incidence of parasystole is approximately 0.13 per cent of all electrocardiograms taken in a general hospital and is seen twice as frequently in males.
  • In the majority of the cases studied with parasystole there was demonstrated some form of heart disease and 65 per cent of the patients were older than 60 years of age.
  • The most commonly associated heart diseases were arteriosclerotic heart disease and/or hypertensive cardiovascular disease (60 per cent) and half of these subjects had congestive heart failure.


  • Patients of all age groups may develop Parasystole.
  • Parasystole is more commonly observed among patients older than 60 years old.
  • Parasystole is more commonly observed among elderly patients.


  • Males are more commonly affected with Parasystole than females.
  • The male to female ratio is approximately 2 to 1.


  • There is no racial predilection for Parasystole.

Risk Factors

  • Parasystole is a kind of arrhythmia caused by the presence and function of a secondary pacemaker in the heart,so any heart rhythm problem or condition can be a risk factor.
  • The most commonly associated heart diseases were arteriosclerotic heart disease and/or hypertensive cardiovascular disease (60 per cent) and half of these subjects had congestive heart failure.
  • Various other acquired and congenital heart diseases were also associated with this arrhythmia but 14 per cent failed to show any evidence of heart disease.

Natural History, Complications and Prognosis

  • Early clinical features include palpitations, shortness of breath, chest pain.
  • Although parasystole generally carries a benign prognosis, parasystolic beats may be capable of inducing ventricular tachycardia and ventricular fibrillation on rare occasions.
  • The prognosis of individuals with arrhythmia is influenced by the presence, absence or status of the underlying heart disease.


  • Diagnosis based on EKG.


  • Symptoms of may include the following:
  • Palpitation
  • Shortness of breath
  • Chest pain
  • Syncope

Laboratory Findings

  • There are no specific laboratory findings associated with parasystole.

Imaging Findings

  • There are no imaging study findings associated with parasystole.

ECG signals

On an ECG, parasystole may be recognized by:

  • spotting ectopic P or QRS waves which either:
    • occur at regular intervals
    • the time between them is always exact multiple of the smallest time between such two occurrences
  • spotting "fusioned" P or QRS complexes (sometimes rare)

Another feature is the varying coupling interval between sinus and ectopic beats.


Medical Therapy

  • There is no treatment for parasystole, the mainstay of therapy is supportive care.


  • Surgery is not an option for parasystole.


  • There are no primary preventive measures available for parasystole.

External links

Template:WikiDoc Sources

  1. Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). "The ECG as a tool to determine atrial fibrillation complexity". Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  2. Harris K, Edwards D, Mant J (2012). "How can we best detect atrial fibrillation?". J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  3. Cosío FG (June 2017). "Atrial Flutter, Typical and Atypical: A Review". Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  4. Katritsis DG, Josephson ME (August 2016). "Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia". Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  5. Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). "Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway". Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  6. "Atrioventricular Nodal Reentry Tachycardia (AVNRT) - StatPearls - NCBI Bookshelf".
  7. Schernthaner C, Danmayr F, Strohmer B (2014). "Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias". Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  8. Scher DL, Arsura EL (September 1989). "Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment". Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  9. Goodacre S, Irons R (March 2002). "ABC of clinical electrocardiography: Atrial arrhythmias". BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  10. Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). "Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome". J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
  11. Strasburger JF, Cheulkar B, Wichman HJ (December 2007). "Perinatal arrhythmias: diagnosis and management". Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
  12. Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). "Evaluation and management of wolff-Parkinson-white in athletes". Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  13. Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). "Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues". Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  14. Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). "Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction". J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  15. Samie FH, Jalife J (May 2001). "Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart". Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  16. Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). "Sudden cardiac death: epidemiology and risk factors". Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  17. Koplan BA, Stevenson WG (March 2009). "Ventricular tachycardia and sudden cardiac death". Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  18. Levis JT (2011). "ECG Diagnosis: Monomorphic Ventricular Tachycardia". Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.