ecg tutorial_ ventricular arrhythmias

7/12/2015 ECG tutorial: Ventricular arrhythmias

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AuthorJordan M Prutkin, MD,MHS, FHRS

Section EditorAry L Goldberger, MD

Deputy EditorGordon M Saperia, MD,FACC

ECG tutorial: Ventricular arrhythmias

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Jun 2015. | This topic last updated: Nov 25, 2013.

INTRODUCTION — Ventricular arrhythmias are wide complex rhythms that may be regular or irregular.These may be normal rate, bradycardic, or tachycardic, and may occur as single beats or sustained. Someventricular arrhythmias may be present as sudden cardiac arrest.

PREMATURE VENTRICULAR CONTRACTIONS — Premature ventricular contractions (PVCs), ventricularpremature beats (VPBs), ventricular premature complexes (VPCs), premature ventricular beats (PVBs), orventricular extrasystoles (VES) are early occurring, widened QRS complexes that have a distinctmorphology (resembling neither a typical left nor right bundle branch block) that is markedly different fromthe sinus QRS complex. Unifocal PVCs all have a single morphology. Multiple different QRS morphologiesare termed multiform PVCs.

In general, there is no P wave identified before a premature QRS complex. However, there may be a normalsinus P wave present if the PVC is very late; in this situation, there is a long coupling interval (from the priorQRS complex), the P wave is not conducted, and the PR interval is shorter than the native sinus beat.

The QRS complex of a PVC is widened, often notched, and with a QRS duration usually >0.16 seconds(waveform 1). It will have a morphology that resembles a right or left bundle branch block depending uponthe location of origin, but its morphology is generally not the same as a typical bundle branch block. It isassumed that the PVC originates in the left ventricle when it has a positive deflection or tall R wave in V1(right bundle branch block configuration), while a negative complex with a deep S wave in V1 (resembling aleft bundle branch block morphology) originates in the right ventricle. Other findings on theelectrocardiogram (ECG) include marked repolarization abnormalities, manifested as ST segment and Twave abnormalities. Retrograde activation of the atrium is variably present; it depends upon the location ofthe premature beat, the time necessary for impulse conduction to the atrioventricular (AV) node, the couplinginterval to the prior sinus beat, and the ability of the node to conduct retrograde to the atrium. When present,there is a retrograde P wave, usually seen within or slightly before the T wave. The interval from theprevious P wave to the retrograde P wave is, however, shorter than the underlying sinus PP interval,reflecting the premature activation of the atrium.

There can be many sinus node responses to a PVC. Most commonly, a full compensatory pause follows thePVC; thus, the PP interval between the QRS complexes before and after the premature beat is twice the PPinterval between two successive sinus beats. The pause is due to retrograde AV nodal penetration of thePVC, which causes the AV node to be refractory to the next ontime sinus impulse, which is blocked. Thesubsequent sinus impulse does conduct through the AV node to stimulate the ventricle. In this situation, anormal appearing P wave may be seen, often buried in the ST segment or T wave of the PVC, with no QRSfollowing it. Other cases may have retrograde activation of the atrium with an inverted P wave in the inferiorleads and resultant delay of sinus node impulse generation. In this situation, the PP interval between theQRS complex before and after the PVC is less than two sinus beats.

On occasion, the PVC may be interpolated. It occurs between two normal sinus QRS complexes, and thePP interval between the QRS complex prior to and after the premature beat is the same as the underlyingsinus PP interval, due to lack of retrograde penetration into the AV node (waveform 2). If the ventricularmyocardium is no longer refractory from the PVC, it is capable of again being stimulated from the next sinusbeat. There also may be concealed retrograde conduction of the PVC into the AV node, rendering it partiallyrefractory and leading to a longer PR interval of the first sinus beat following the premature complex.

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Ventricular bigeminy — Ventricular bigeminy is present when a premature ventricular complex followseach sinus beat (waveform 3). Ventricular bigeminy may become selfperpetuating, a situation known as therule of bigeminy. This occurs because the long cycle length after the prior PVC tends to precipitate the nextPVC after a sinus beat. The presence of ventricular bigeminy indicates a repeating pattern but has no otherclinical implications.

Ventricular trigeminy — Ventricular trigeminy is present when two sinus beats are followed by theventricular premature beat. Thus, every third beat is a ventricular premature beat (waveform 4).

Ventricular couplets — Ventricular couplets are defined as two PVCs in a row (waveform 5). There is oftena compensatory pause after the second premature beat. The two premature beats may have an identicalmorphology (unifocal couplet), or their morphology may differ (multifocal couplet). The RR interval betweenthe two successive PVCs varies widely.

VENTRICULAR ESCAPE COMPLEXES OR RHYTHM — An escape ventricular beat or rhythm occurswhen there is failure of the sinus and atrioventricular (AV) node to generate an impulse. There is an absenceof P wave activity, associated with a widened QRS complex that resembles a premature ventricularcontraction (PVC) and occurs after a pause of variable duration (but always greater than the normal sinusRR interval). Persistence of this activity leads to multiple successive ventricular complexes, representing anescape ventricular rhythm with a rate that is slower than the normal sinus rhythm. In cases of complete orthird degree heart block in which there is sinus node activity but failure of conduction through the AV node,there are P waves dissociated from the ventricular complexes with a rate faster than the ventricular rate (AVdissociation) (waveform 6).

VENTRICULAR PARASYSTOLE — Ventricular parasystole represents an independent ectopic ventricularrhythm that has no relationship to the sinus rhythm. It appears on the electrocardiogram (ECG) as unifocalpremature ventricular contractions (PVCs) with a variable coupling cycle (the interval between the prior sinusbeat and the premature beat varies) (waveform 7). The interval between two successive PVCs is alwaysconstant or some integer of the underlying rate of the ectopic focus.

Ventricular parasystole is the result of an ectopic focus within the ventricular myocardium or ventricularconduction system, which manifests spontaneous automaticity and has a rate that is slower than theunderlying sinus rate. This focus is not depressed or overdriven by the normal ventricular conductionbecause of entrance block into the area of the ectopic focus; it is protected from suppression. However, theectopic focus may or may not activate the ventricular myocardium and therefore result in a PVC, dependingon the ability of the rest of the ventricular myocardium to be stimulated, which in turn is determined by itsstate if refractoriness. Thus, there may also be intermittent exit block from this focus, and the PVC does notappear at the expected time, but later PVCs are present at the underlying rate of the parasystolic focus.

VENTRICULAR TACHYCARDIA — Ventricular tachycardia (VT) is defined as three or more successiveventricular complexes at a rate greater than 100 beats per minute. Nonsustained VT is a series of at leastthree consecutive ventricular beats that have a duration of less than 30 seconds or do not requireemergency intervention; sustained VT lasts for more than 30 seconds or requires termination early becauseof hemodynamic impairment. The rhythm is usually regular, although there may be slight irregularity of theRR intervals. (See "Nonsustained VT in the absence of apparent structural heart disease" and "Sustainedmonomorphic ventricular tachycardia: Diagnosis and evaluation".)

The morphology of the QRS complex during VT is usually different when compared to the sinus beat. (See"Approach to the diagnosis of wide QRS complex tachycardias".)

Additionally, it does not resemble either a typical left or right bundle branch block, as ventricular activation isnot via the normal HisPurkinje conduction system, but is through direct ventricular myocardial activation.The QRS axis may be deviated to the left or to the right. The width of the QRS complex is generally >0.16sec when in a left bundle branch block pattern and >0.14 sec when in a right bundle branch block pattern.Other useful features of ventricular tachycardia include:

Atrioventricular (AV) dissociation, which is the hallmark of ventricular tachycardia. Subtle differences inSTT wave morphology representing possibly superimposed P waves should be assessed.






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The VT is monomorphic when all of the QRS complexes of an episode are identical (waveform 8). However,monomorphic VT often displays subtle changes of the QRS complexes with regard to morphology and widthas a result of variable changes in the electrophysiologic properties of the ventricular myocardium.

When the QRS complexes within each episode display changing morphologies, often with grossly irregularRR intervals, the VT is called polymorphic (waveform 9). (See "Catecholaminergic polymorphic ventriculartachycardia and other polymorphic ventricular tachycardias with a normal QT interval".) The differences inQRS morphology result from changes in the direction (vector) of myocardial activation due to markedheterogeneity of the electrophysiologic characteristics of the ventricular myocardium. The rate is usuallybetween 100 and 330 beats per minute. If the polymorphic VT is associated with a baseline QRS complexthat has a normal QT interval, the most common etiology is ischemia. If the polymorphic VT is associatedwith a QRS complex on the baseline electrocardiogram (ECG) that has QT prolongation, then thepolymorphic VT is termed “torsades des pointes.” The QT prolongation may be acquired, due to medicationsthat prolong the QT interval (see "Acquired long QT syndrome") or congenital, the result of a channelopathy(see "Clinical features of congenital long QT syndrome").

The presence of AV dissociation is a very important finding and is usually diagnostic of VT. (See "Approachto the diagnosis of wide QRS complex tachycardias".) However, it is not always present, or if present maynot be easily recognized, especially when the ventricular rate is very rapid (the RR cycle length is short). TheP waves are not distinctive in these cases, but may alter the QRS complexes or be superimposed upon theST and T waves, causing irregular changes in their morphology.

AV dissociation occurs as a result of retrograde VA conduction that enters, but blocks, within the AV node(concealed conduction). The retrograde concealed conduction into the node causes the node to berefractory to antegrade stimulation, thereby blocking conduction from the atrium to the ventricle. If thetachycardia does not lead to AV block, fusion or capture beats may be present, as described below. In somecases of VT, there is retrograde conduction through the AV node and retrograde activation of the atria.There may be a variable degree of retrograde block (2:1, 3:1, or even Wenckebach); on occasion, there maybe 1:1 retrograde activation of the atrium and therefore no AV dissociation with a fixed RP interval.Dissociation is more obvious when the tachycardia rate is relatively slow. The P waves occur at a slowerrate than the QRS complexes, and there is no relationship between them.

Other features of AV dissociation include:

Presence of fusion or capture beats.

Absence of an RS complex in all of the precordial leads.

Longest R to S interval >100 ms in any precordial lead.

Concordance of the QRS complex across the precordial leads (eg, R waves or S waves only in leadsV1V6). However, this may be seen in any situation in which there is direct myocardial activation,including WolffParkinsonWhite pattern or a paced complex. Negative concordance is less useful, asthis may be seen with a left bundle branch block.

A monophasic Rr' pattern in lead 1 (termed rabbit ears) with a taller left ear. This is often associatedwith an rS or QS complex morphology in leads V5V6.

An indeterminate axis (between 90 and 180º). However, this may be seen in any situation in whichthere is direct myocardial activation including a paced rhythm (especially biventricular pacing) or WolffParkinsonWhite pattern.

In lead II, time from beginning of the QRS to first change of polarity ≥50ms, regardless of whether theQRS change is positive or negative.

In lead aVR, an initial R wave, width of the r or q wave >40ms, and/or notch on the descending limb ofa predominantly negative QRS.

Fusion beats, which occur with a QRS complex that has features resembling both the sinus QRS andthat of the VT. These result from simultaneous activation of the ventricles from the ventricular focus as


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Repetitive monomorphic ventricular tachycardia — Repetitive monomorphic VT occurs in those with nostructural heart disease. (See "Monomorphic ventricular tachycardia in the absence of apparent structuralheart disease".)

It most frequently originates from the right ventricular outflow tract (RVOT) just inferior to the pulmonaryvalve, but less frequently may occur in the left ventricular outflow tract, sinuses of Valsalva, or other areas ofthe heart. RVOT VT has the ECG appearance of a left bundle branch block pattern with an inferiorly directedaxis. In general, these have a benign prognosis.

Ventricular flutter — Ventricular flutter is a monomorphic VT that occurs at a very rapid rate, usually around300 beats per minute (figure 1). Often no distinctive T waves are discernible. There is no isoelectric intervalbetween QRS complexes. P waves or evidence of atrial activity are absent since the ventricular rate is rapid.

Torsades de pointes — Torsades de pointes is a rapid and distinct form of polymorphic VT associated witha baseline prolonged QT interval. It means "twisting of points," a name that refers to the continuouslychanging axis of polymorphic QRS morphologies that are observed during each episode (waveform 11AB).The typical form is initiated by bradycardia or is pause dependent, with a shortlongshort coupling interval,ie, a PVC (short RR interval), a compensatory pause (long RR interval), and second PVC (short RR interval)(waveform 11B). (See "Clinical features of congenital long QT syndrome".) If the baseline QTc interval isnormal, the rhythm is referred to as polymorphic VT and not torsades de pointes.

ACCELERATED IDIOVENTRICULAR RHYTHM — An accelerated idioventricular rhythm (AIVR) is arepetitive ventricular rhythm occurring at a rate between 60 and 100 beats per minute (waveform 12). It maybe the result of an accelerated ventricular focus that generates an impulse faster than the sinus node andtherefore assumes control. There may or may not be atrioventricular (AV) dissociation; if dissociation ispresent, the atrial rate is slower than the ventricular rate and the PP intervals are longer than the RRintervals. On the other hand, if the idioventricular rhythm represents an escape rhythm (generally the resultof third degree AV nodal block), the P waves are dissociated from the QRS impulses and the atrial rate isfaster than the ventricular rate. In the setting of acute ischemia, AIVR may be a marker of spontaneous orinduced reperfusion. (See "Third degree (complete) atrioventricular block".)

VENTRICULAR FIBRILLATION — Ventricular fibrillation is identified by the complete absence of properlyformed QRS complexes and no obvious P waves (waveform 13). There is no uniform activation of theventricular myocardium and the QRS complexes have markedly different morphology, axis, and amplitude.The rate is irregular and usually greater than 300 beats per minute. When the fibrillation is recent onset, theamplitude is usually high, but as time passes, the fibrillatory waves become finer and may resembleasystole. Ventricular fibrillation leads promptly to cardiac arrest.

SUMMARY

well as via a sinus beat travelling down the normal AV nodalHis Purkinje pathway.

Capture or Dressler beats, which are intermittently captured QRS complexes that are identical to sinuscomplexes. They are preceded by a P wave, indicating that there is intermittent capture of theventricles by the sinus node via the normal AV nodalHis Purkinje pathway (waveform 10). However,the occurrence of intermittent capture of the ventricle from above does not alter the VT or affect itsfocus of origin.

Premature ventricular contractions (PVCs) are early occurring beats with widened QRS complexes thathave a distinct morphology that is markedly different from the sinus QRS complex (waveform 1). Othercharacteristics include marked repolarization abnormalities and no conducted P wave identified beforea premature QRS complex.

Ventricular tachycardia (VT) is defined as three or more successive ventricular complexes (waveform8). Nonsustained VT is a series of at least three repetitive ventricular beats that have a duration of lessthan 30 seconds or do not require emergency therapy; sustained VT lasts for more than 30 seconds oris terminated earlier because of hemodynamic impairment. If there is one basic morphology of the QRScomplexes, it is termed “monomorphic VT.” If the QRS complex morphology is changing, especially

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Topic 2119 Version 5.0

with a change in axis, the VT is termed “polymorphic.” Polymorphic VT associated with a baseline longQTc is called torsades de pointes.

An accelerated idioventricular rhythm (AIVR) is a repetitive ventricular rhythm occurring at a ratebetween 60 and 100 beats per minute (waveform 12).

Ventricular fibrillation is identified by the complete absence of properly formed QRS complexes and noobvious P waves (waveform 13). This leads to sudden cardiac arrest.



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GRAPHICS

Single lead electrocardiogram (ECG) showing aventricular premature beat (VPB)

The fourth beat is a ventricular premature beat (VPB). It has a wide,bizarre morphology, with a duration >0.16 seconds.

Graphic 57511 Version 3.0

Sinus rhythm

The normal P wave in sinus rhythm is slightly notched since activationof the right atrium precedes that of the left atrium. The P wave isupright in a positive direction in leads I and II. A P wave with auniform morphology precedes each QRS complex. The rate is between60 and 100 beats per minute and the cycle length is uniform betweensequential P waves and QRS complexes. In addition, the P wavemorphology and PR intervals are identical from beat to beat.




Single lead electrocardiogram (ECG) showing aninterpolated ventricular premature beat (VPB)

The third beat is a ventricular premature beat (VPB). It is called aninterpolated VPB since it does not alter the underlying sinus RR interval.


Sinus rhythm





Electrocardiogram (ECG) showing ventricular bigeminy

A ventricular premature beat (VPB) follows each sinus beat, and the couplinginterval between the VPB and the previous sinus QRS complex is constant (fixedcoupling interval). The resulting pattern is referred to as ventricular bigeminy.


Sinus rhythm





Single lead electrocardiogram (ECG) showing ventriculartrigeminy

Every third beat is a ventricular premature beat (VPB). The coupling intervalbetween the VPB and the previous sinus QRS complex is constant (fixedcoupling interval). The resulting pattern is referred to as ventricular trigeminy.


Sinus rhythm




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Ventricular couplet

Two ventricular premature beats (VPBs) occur following three normal QRScomplexes. This is a unifocal couplet since both VPBs have the samemorphology.


Sinus rhythm





Complete heart block: Sinus rhythm with slow junctionalor idioventricular escape rhythym

Multiple successive QRS complexes appear that are of ventricular origin andoccur at a rate which is slower than the underlying sinus rhythm. The presenceof P waves that occur independent of the QRS complexes is evidence ofatrioventricular dissociation.


Sinus rhythm





Electrocardiogram (ECG) showing ventricularparasystole

Unifocal parasystolic ventricular premature beats (VPBs) occur at a ratewhich is slower than the underlying sinus rhythm and manifest differentcoupling intervals (ie, the distance between the VPB and the prior QRScomplex). The ectopic focus does not always activate the ventricularmyocardium (and therefore does not produe a VPB and the ECG) since itmay arrive at a time when the ventricle is refractory due to activationfrom the normal conduction pathway. However, the interval between twosuccessive VPBs is always some integer of the underlying rate of theectopic focus (the interectopic intervals have a common denominator)since the ectopic focus is undisturbed and continues to fire at its ownintrinsic rate.


Sinus rhythm





Single lead electrocardiogram (ECG) showingmonomorphic ventricular tachycardia

Three or more successive ventricular beats are defined as ventriculartachycardia (VT). This VT is monomorphic since all of the QRS complexeshave an identical appearance. Although the P waves are not distinct, they canbe seen altering the QRS complex and STT waves in an irregular fashion,indicating the absence of a relationship between the P waves and the QRScomplexes, ie, AV dissociation is present.


Normal rhythm strip

Normal rhythm strip in lead II. The PR interval is 0.15 sec and theQRS duration is 0.08 sec. Both the P and T waves are upright.

Courtesy of Morton F Arnsdorf, MD.




Single lead electrocardiogram (ECG) showingpolymorphic ventricular tachycardia (VT)

The QRS complexes in polymorphic VT have markedly differingmorphologies due to changes in the direction (vector) of myocardialactivation.


Normal rhythm strip






Fusion beats

The rhythm strip in a patient with sustained ventricular tachycardia shows afusion beat and a capture beat. The fusion beat occurs when a supraventricularimpulse (following the first P wave) causes ventricular activation, which fuseswith the complex originating in the ventricle, producing a hybrid complex. Thecomplex following the second P wave has the appearance of a normal QRScomplex and is known as a capture beat.


Normal rhythm strip






Ventricular flutter

A rapid ventricular tachycardia, with rates usually over 240 beats perminute, is characteristic of ventricular flutter, with predominantlymonomorphic QRS complexes, and an absence of atrial activity (Pwaves).


Sinus rhythm





Single lead electrocardiogram (ECG) showingtorsades de pointes

This is an atypical, rapid, and bizarre form of ventricular tachycardiathat is characterized by a continuously changing axis of polymorphicQRS morphologies.




Single lead electrocardiogram (ECG) showingtorsades de pointes

The electrocardiographic rhythm strip shows torsades de pointes, apolymorphic ventricular tachycardia associated with QT prolongation.There is a short, preinitiating RR interval due to a ventricular couplet,which is followed by a long, initiating cycle resulting from thecompensatory pause after the couplet.




Single lead electrocardiogram (ECG) showing acceleratedidioventricular rhythm

An accelerated ventricular rhythm occurs in this case at a rate of 70 beats/minute.The P waves are dissociated from the QRS complexes and occur at rate which isslower than the RR interval.


Normal rhythm strip






Single lead electrocardiogram (ECG) showingventricular fibrillation

There is a complete absence of properly formed QRS complexes and noobvious P waves. A recent onset (eg, within minutes) of the arrhythmia issuggested by the coarse morphology of the fibrillatory waves.


Normal rhythm strip






Disclosures: Jordan M Prutkin, MD, MHS, FHRS Grant/Research/Clinical Trial Support: BostonScientific [Heart block (Pacemakers and ICDs)]; St. Jude Medical [Sudden death (Pacemakers andICDs)]. Ary L Goldberger, MD Nothing to disclose. Gordon M Saperia, MD, FACC Nothing to disclose.Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these areaddressed by vetting through a multilevel review process, and through requirements for references to beprovided to support the content. Appropriately referenced content is required of all authors and mustconform to UpToDate standards of evidence.Conflict of interest policy

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