Parasystole

WikiDoc Resources for Parasystole
Articles
Most recent articles on Parasystole Most cited articles on Parasystole Review articles on Parasystole Articles on Parasystole in N Eng J Med, Lancet, BMJ
Media
Powerpoint slides on Parasystole Images of Parasystole Photos of Parasystole Podcasts & MP3s on Parasystole Videos on Parasystole
Evidence Based Medicine
Cochrane Collaboration on Parasystole Bandolier on Parasystole TRIP on Parasystole
Clinical Trials
Ongoing Trials on Parasystole at Clinical Trials.gov Trial results on Parasystole Clinical Trials on Parasystole at Google
Guidelines / Policies / Govt
US National Guidelines Clearinghouse on Parasystole NICE Guidance on Parasystole NHS PRODIGY Guidance FDA on Parasystole CDC on Parasystole
Books
Books on Parasystole
News
Parasystole in the news Be alerted to news on Parasystole News trends on Parasystole
Commentary
Blogs on Parasystole
Definitions
Definitions of Parasystole
Patient Resources / Community
Patient resources on Parasystole Discussion groups on Parasystole Patient Handouts on Parasystole Directions to Hospitals Treating Parasystole Risk calculators and risk factors for Parasystole
Healthcare Provider Resources
Symptoms of Parasystole Causes & Risk Factors for Parasystole Diagnostic studies for Parasystole Treatment of Parasystole
Continuing Medical Education (CME)
CME Programs on Parasystole
International
Parasystole en Espanol Parasystole en Francais
Business
Parasystole in the Marketplace Patents on Parasystole
Experimental / Informatics
List of terms related to Parasystole

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

Overview

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.

Classification

• 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.

Pathophysiology

• 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.

• Atrial fibrillation is irregularly irregular, while the other rhythms such as atrial flutter, sinus tachycardia, AV nodal reentry tachycardia and paroxysmal supraventricular tachycardia are all much more regular.
• An atrioventricular nodal reentry tachycardia will often break with either carotid sinus massage or AV nodal blocking agents.
• If the patient has Wolff-Parkinson-White syndrome there may be much more rapid conduction. The presence of the delta wave on EKG is characteristic.

Arrhythmia	Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrial Fibrillation (AFib)	Irregularly irregular	On a 10-second 12-lead EKG strip, multiply number of QRS complexes by 6	Absent Fibrillatory waves	Absent	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Does not break with adenosine or vagal maneuvers	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	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement
Atrial Flutter	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	Incidence: 88 per 100,000 individuals	Elderly Alcohol
Atrioventricular nodal reentry tachycardia (AVNRT)	Regular	140-280 bpm	Slow-Fast AVNRT: Pseudo-S wave in leads II, III, and AVF Pseudo-R' in lead V1. Fast-Slow AVNRT P waves between the QRS and T waves (QRS-P-T complexes) Slow-Slow AVNRT Late P waves after a QRS Often appears as atrial tachycardia. 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	May break with adenosine or vagal maneuvers	60%-70% of all supraventricular tachycardias	Structural heart disease Atrial tachyarrhythmias
Multifocal Atrial Tachycardia	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	Variable PR intervals, RR intervals, and PP intervals	Less than 0.12 seconds, consistent, and normal in morphology	Does not terminate with adenosine or vagal maneuvers	0.05% to 0.32% of electrocardiograms in general hospital admissions	Elderly Chronic obstructive pulmonary disease (COPD)
Paroxysmal Supraventricular Tachycardia	Regular	150 and 240 bpm	Absent Hidden in QRS	Absent	Narrow complexes (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex	Prevalence: 0.023 per 100,000	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome
Premature Atrial Contractrions (PAC)	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: PAC displaying a right bundle branch block pattern	Usually narrow (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex		Infants Cardiomyopathy Myocarditis Elderly Coronary artery disease Stroke Increased atrial natriuretic peptide (ANP) Hypercholesterolemia
Wolff-Parkinson-White Syndrome	Regular	Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm	With orthodromic conduction due to a bypass tract, the P wave generally follows the QRS complex, whereas in AVNRT, the P wave is generally buried in the QRS complex.	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.	May break in response to procainamide, adenosine, vagal maneuvers	Worldwide prevalence of WPW syndrome is 100 - 300 per 100,000	Ebstein's anomaly Mitral valve prolapse: This cardiac disorder, if present, is associated with left-sided accessory pathways. Hypertrophic cardiomyopathy: This disorder is associated with familial/inherited form of WPW syndrome. Hypokalemic periodic paralysis Pompe disease Tuberous sclerosis
Ventricular Fibrillation (VF)	Irregular	150 to 500 bpm	Absent	Absent	Absent (R on T phenomenon in the setting of ischemia)	Does not break in response to procainamide, adenosine, vagal maneuvers	3-12% cases of acute myocardial infarction (AMI) Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm	Myocardial ischemia / infarction Cardiomyopathy Channelopathies e.g. Long QT (acquired / congenital) Electrolyte abnormalities (hypokalemia/hyperkalemia, hypomagnesemia) Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis) Sepsis Hypothermia Pneumothorax Seizures Stroke
Ventricular Tachycardia	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	Does not break in response to procainamide, adenosine, vagal maneuvers	5-10% of patients presenting with AMI	Coronary artery disease Aortic stenosis Cardiomyopathy Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) Inherited channelopathies (e.g., long-QT syndrome) Catecholaminergic polymorphic ventricular tachycardia Arrhythmogenic right ventricular dysplasia Myocardial infarction Torsades de pointes is a form of polymorphic VT that is often associated with a prolonged QT interval

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.

Age

• 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.

Gender

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

Race

• 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

• Diagnosis based on EKG.

Symptoms

• 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.

Treatment

Medical Therapy

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

Surgery

• Surgery is not an option for parasystole.

Prevention

• There are no primary preventive measures available for parasystole.

External links

• ventricular parasystole
• atrial parasystole