1. Ventricular arrhythmias
Mehdi Bakhshi
MSN.PhD

2. Take home points
PVCs are very common arrhythmias that can occur in healthy or diseased hearts with multiple features on ECG
VT and VF are dangerous arrhythmias that can lead to sudden cardiac death
Not all wide complex tachyarrhythmias arise from the ventricles
Distinguish between VT and SVT with aberrancy because the treatment and prognosis of each is very different

3. Ventricular arrhythmias
Commonly occur as a result of ectopic focus/foci distal to the bundle of His
Most common one is the premature ventricular contraction (PVC)
Most are benign but can be lethal

4. Mechanisms of ventricular arrhythmias
Impulse Formation Disorders
Abnormal Automaticity
Discharge from a pathologic ectopic ventricular focus
Triggered beats
Afterdepolarizations (AD): Abnormal depolarizations of myocytes that interrupt phase 2, 3, or 4 of the AP
Impulse Conduction Disorders
Delayed conduction
Delayed SA/AV nodal impulse allows initiation of inherent ventricular impulse
Re-entry
Creation of a circuit that leads to 2 or more depolarizations in surrounding tissue
Triggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. These are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).
Reentry occurs when an area of 1-way block in the Purkinje fibers and a second area of slow conduction are present. This condition is frequently seen in patients with underlying heart disease that creates areas of differential conduction and recovery due to myocardial scarring or ischemia. During ventricular activation, the area of slow conduction activates the blocked part of the system after the rest of the ventricle has recovered, resulting in an extra beat. Reentry can produce single ectopic beats ,or it can trigger paroxysmal tachycardia.

5. Afterdepolarization Early afterdepolarization (EAD)
occurs with abnormalities during phase 2 (interrupted due to augmented opening of Ca channels) or phase 3 (opening of Na channels)
Delayed afterdepolarization (DAD)
begin during phase 4 - after repolarization is completed, but before another action potential would normally occur. Due to elevated cytosolic Ca concentrations (digoxin toxicity)
Class Ia agents
Class Ia agent decreasing Vmax, thereby increasing action potential duration.
Class Ia agents block the fast sodium channel. Blocking this channel depresses the phase 0 depolarization (reduces Vmax), which prolongs the action potential duration by slowing conduction. Agents in this class also cause decreased conductivity and increased refractoriness.
Indications for Class Ia agents are supraventricular tachycardia, ventricular tachycardia, symptomatic ventricular premature beats, and prevention of ventricular fibrillation.
Procainamide can be used in the treatment of atrial fibrillation in the setting of Wolff-Parkinson-White syndrome, and in the treatment of wide complex hemodynamically stable tachycardias.
While procainamide and quinidine may be used in the conversion of atrial fibrillation to normal sinus rhythm, they should only be used in conjunction with an AV node blocking agent (ie: digoxin, verapamil, or a beta blocker), because procainamide and quinidine can increase the conduction through the AV node and may cause 1:1 conduction of atrial fibrillation, causing an increase in the ventricular rate.
Class Ia agents include quinidine, procainamide and disopyramide.
Class III agents predominantly block the potassium channels, thereby prolonging repolarization.[7] Since these agents do not affect the sodium channel, conduction velocity is not decreased. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias. (The re-entrant rhythm is less likely to interact with tissue that has become refractory).
Class III antiarrhythmic agents exhibit reverse use dependent prolongation of the action potential duration (Reverse use-dependence). This means that the refractoriness of the ventricular myocyte increases at lower heart rates. This increases the susceptibility of the myocardium to (EADs) at low heart rates. Antiarrhythmic agents that exhibit reverse use-dependence are more efficacious at preventing a tachyarrhythmia than converting someone into normal sinus rhythm. Because of the reverse use-dependence of class III agents, at low heart rates class III antiarrhythmic agents may paradoxically be more arrhythmogenic.
medresidents.stanford.edu/TeachingMaterials/EKGs%20and%20Arrhythmias/Arrythmias%20and%20EKGs%203.ppt

6. Types Premature ventricular contraction (PVC)
Bigeminy, trigeminy, couplets, interpolated, monomorphic, multimorphic, fusion beat
Idioventricular rhythm/ accelerated idioventricular rhythm
Ventricular parasystole
Ventricular tachycardia (VT)
Torsades de pointes
Ventricular flutter
Ventricular fibrillation (VF)

7. Premature Ventricular Contractions (PVCs)
Epidemiology
Very common; occur in healthy people & pts with cardiac disease
Etiology
Cardiac: CAD, post-MI, MVP, CHF, rheumatic heart disease, congenital arrhythmias
Non-cardiac: acid-base disturbance, electrolyte abnormalities, meds, caffeine, anxiety
Symptoms
Palpitations, “skipped beats”
Chest or neck discomfort
Physical exam findings
Presence of premature beat
Hypotension
Decreased or absent peripheral pulses (radial)
Patients are usually asymptomatic.
Cannon A waves or the increased force of contraction due to postextrasystolic potentiation of contractility can cause palpitations and neck and/or chest discomfort.
The patient may report feeling that his or her heart "stops" after a PVC.
Patients with frequent PVCs or bigeminy may report syncope. This symptom is due to either inadequate stroke volume or decreased cardiac output caused by the condition effectively halving the heart rate.
Long runs of PVCs can result in hypotension.
Exercise can increase or decrease the PVC rate.

8. ECG Characteristics of PVCs
Ectopic beat originating from ventricles occurring before next expected beat (premature)
Usually not proceeded by P wave
Wide QRS: at least > 0.12 sec, usually with bizarre morphology
Large T wave in the opposite direction of the major QRS deflection

9. ECG Characteristics of PVCs
Full Compensatory Pause
Follows most PVCs
PVCs usually do not conduct retrograde to the atria, thus SA nodal rhythm not disturbed
When SA node discharges, the ventricles are still refractory from the PVC and don’t depolarize in response to the impulse
The interval between the first sinus beat and the PVC plus the interval between the PVC and the next sinus beat = 2 normal sinus intervals
complete compensatory pause because the sinus node timing is not interrupted; one sinus P wave isn't able to reach the ventricles because they are still refractory from the PVC; the following sinus impulse occurs on time based on the sinus rate. In contrast, PACs are usually followed by an incomplete pause because the PAC usually enters the sinus node and resets its timing; this enables the following sinus P wave to appear earlier than expected. These concepts are illustrated below.

10. ECG Characteristics of PVCs
Interpolated PVCs
No compensatory pause
PVC occurs between 2 normal sinus beats
No change in the R-R interval
Usually seen when the HR is slow

11. ECG Characteristics of PVCs
Fusion beats
Simultaneous activation of the ventricle from supraventricular impulse and a PVC
Ventricular depolarization occurs simultaneously in two directions
QRS complex that has the characteristics of the PVC and the QRS complex of the underlying rhythm
Captured beats (Dressler beats)
QRS complexes during a WCT that are identical to the sinus QRS complex.
Implies that the normal conduction system has momentarily "captured" control of ventricular activation from the VT focus.

12. ECG Characteristics of PVCs
R on T phenomenon
PVC begins during mid/late T wave
Associated with vulnerable ventricles often predisposing to polymorphic VT or VF, especially in acute ischemia

13. PVC Patterns Bigeminy Trigeminy Couplets Triplets PVC every other beat
“Rule of bigeminy”: often becomes self-perpetuating
Trigeminy
PVC every 3rd beat
Couplets
Two successive PVCs
Triplets
Tree successive PVCs
Rate <100bpm

14. PVC Morphology Monomorphic Polymorphic
PVCs originate from a single ventricular ectopic focus
Single wave morphology
Polymorphic
PVCs origniate from multiple ventricular ectopic foci
≥ 2 morphologies

15. PVC Prognosis and Treatment
Lown Classification
Class 1: <30PVC/hr
Class 2: >30 PVC/hr
Class 3: Multiform PVCs
Class 4a: PVC couplets
Class 4b: PVC triplets or greater
Class 5: R on T
Post MI PVCs and Lown’s class 3-5 are associated with ↑ risk for VT/VF and sudden death
Treatment
No changes in mortality with PVC suppressive tx
Asx, healthy: reassurance
Sx: B-Blockers

16. Idioventricular (Escape) rhythm
Escape rhythm due to failure of SA/AVN ventricular activation or complete conduction block
Inherent 20-40bpm takes over since it is no longer suppressed
Regular wide QRS
Etiologies
Post-MI, CM, digoxin toxicity
Multiple successive QRS complexes appear that are of ventricular origin and occur at a rate which is slower than the underlying sinus rhythm. The presence of P waves that occur independent of the QRS complexes is evidence of atrioventricular dissociation.
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 is slower than the RR interval.
Idioventricular Rhythm
 A "passive" escape rhythm that occurs by default whenever higher-lever pacemakers in AV junction or sinus node fail to control ventricular activation.  Escape rate is usually bpm (i.e., slower than a junctional escape rhythm).  Seen most often in complete AV block with AV dissociation or in other bradycardic conditions.
ACCELERATED IDIOVENTRICULAR RHYTHM — An accelerated idioventricular rhythm (AIVR) is a repetitive ventricular rhythm occurring at a rate between 60 and 100 beats per minute (show ECG 13). It may be the result of an accelerated ventricular focus which generates an impulse faster than the sinus node and therefore assumes control. There may or may not be AV dissociation; if dissociation is present, the atrial rate is slower than the ventricular rate and the PP intervals are therefore longer than the RR intervals. On the other hand, if the idioventricular rhythm represents an escape rhythm (generally the result of third degree AV nodal block), the P waves are dissociated from the QRS impulses and the atrial rate is faster than the ventricular rate. (See "Third degree (complete) atrioventricular block").

17. Accelerated Idioventricular Rhythm (AIVR)
Sinus bradycardia
AIVR
May result from accelerated ventricular focus that is faster than the prevailing sinus rate and takes over or can occur as escape rhythm ( generally with 3rd degree AVN block)
Usually bpm (differentiates from VT)
Regular wide QRS
Associated with post-MI (especially inferior wall MI), reperfusion tx, digoxin toxicity, or after a PVC
Usually self limited, rarely see progression to VT/VF
Enhanced automaticity appears to be the likely electrophysiologic mechanism behind the genesis of AIVR. Enhanced automaticity generally is ascribed to phase-4 depolarization of the action potential of the myocardial cell. AIVR can occur in the His-Purkinje fibers or myocardium under certain abnormal metabolic conditions.
AIVR arises from subordinate or second-order pacemakers and manifests itself when the patient's prevailing sinus rate becomes lower than the accelerated rate (AIVR) of the otherwise suppressed focus. Sinus bradycardia combined with enhanced automaticity of the subordinate site is the common pathophysiology.
Several conditions, including myocardial ischemia (especially inferior wall ischemia or infarction), digoxin toxicity, electrolyte imbalance (eg, hypokalemia), and hypoxemia may accentuate the phase-4 depolarization in the subordinate pacemaker tissues of the atrioventricular (AV) junction or His-Purkinje system, thus increasing the rate of impulse generation. Frequently, when inferior wall ischemia is present, the subordinate pacemaker acceleration coexists with sinus node depression. The latter permits escape and domination of the pacemaker function, which may occur with AV junctional or ventricular rates of only bpm. The ectopic mechanism also can begin after a premature ventricular complex or, as described above, when the ectopic ventricular focus simply can accelerate sufficiently enough to overtake the intrinsic rhythm.
The onset of AIVR is gradual (nonparoxysmal). The ventricular rhythm can be regular or irregular and, occasionally, can show sudden doubling, suggesting the presence of exit block. The ventricular rate, commonly bpm, usually stays within beats of the sinus rate; therefore, the control of the cardiac rhythm occasionally passes back and forth between these 2 competing pacemaker sites.
Fusion beats often develop at the onset and termination of arrhythmia, which occurs when the pacemakers are competing for control of ventricular depolarization. Because of the slow rate, capture beats also are common. Due to the slow rate and nonparoxysmal onset, precipitation of more rapid ventricular arrhythmias rarely is observed. Rhythm termination generally occurs gradually, while the underlying sinus rhythm accelerates or the AIVR slows down.

18. Ventricular parasystole
Independent ectopic ventricular rhythm competing with the sinus rhythm
May or may not activate the ventricles
Rate slower than sinus, but NOT overdriven because of entrance block
Sinus rhythm unable to enter the ectopic site and reset its timing
Unifocal PVCs with a variable coupling intervals
Interectopic intervals are multiple of the basic rate (e.g. R-R)
Parasystole: Parasystole occurs when a protected focus discharges independently of the dominant pacemaker. The characteristics of parasystole include wide QRS complexes with a varying coupling interval between the ectopic (parasystolic) and the dominant (usually sinus) complex, fusion beats, and variable coupling interval.
Non-fixed coupled PVCs where the inter-ectopic intervals (i.e., timing between PVCs) are some multiple (i.e., 1x, 2x, 3x, etc.) of the basic rate of the parasystolic focus  PVCs have uniform morphology unless fusion beats occur  Usually entrance block is present around the ectopic focus, which means that the primary rhythm (e.g., sinus rhythm) is unable to enter the ectopic site and reset its timing.  May also see exit block; i.e., the output from the ectopic site may occasionally be blocked (i.e., no PVC when one is expected).  Fusion beats are common when ectopic site fires while ventricles are already being activated from primary pacemaker

19. Ventricular Tachycardia (VT)
Life threatening arrhythmia
May lead to VF and sudden death
Etiologies
Heart disease (prior MI, CAD, CM, valvular dz)
ECG findings
≥3 consecutive PVCs with a rate of bpm
No P waves
QRS axis -30° to -180°
AV dissociation
Fusion beats and captured beats
Duration
Non-sustained: <30sec
Sustained: >30 sec or requiring termination because of hemodynamic collapse
Positive or negative concordance of the QRS complex across the precordial leads (eg, R waves or S waves only)
A monophasic Rr' pattern in lead 1 (termed rabbit ears) with a taller left ear.
AV dissociation occurs as a result of retrograde VA conduction but block within the AV node (concealed conduction).
AV dissociation is widely used as a general term for any arrhythmia in which the atria and ventricles are controlled by independent pacemakers. The definition includes complete heart block, as well as some instances of ventricular tachycardia in which the atria remain in sinus rhythm (see Chapter 16 ).
AV dissociation is also used as a more specific term to describe a particular family of arrhythmias that are often mistaken for complete heart block. With this type of AV dissociation, the SA node and AV junction appear to be “out of synch”; thus the SA node loses its normal control of the ventricular rate. As a result, the atria and ventricles are paced independently—the atria from the SA node, the ventricles from the AV junction. This situation is similar to what occurs with complete heart block. With AV dissociation, however, the ventricular rate is the same as or slightly faster than the atrial rate. When the atrial and ventricular rates are almost the same, the term isorhythmic AV dissociation is used. (Iso is the Greek root for “same.”)
The critical difference between AV dissociation (resulting from “desynchronization” of the SA and AV nodes) and actual complete heart block (resulting from true conduction failure) is as follows: with AV dissociation (e.g., isorhythmic) a properly timed P wave can be conducted through the AV node, whereas with complete heart block no P wave reaches the ventricles.
AV dissociation ( Fig ) therefore can be regarded as a “competition” between the SA node and the AV node for control of the heartbeat. It may occur either when the SA node slows down (e.g., because of the effects of beta blockers or calcium channel blockers or with increased vagal tone) or when the AV node is accelerated (e.g., by ischemia or digitalis toxicity). Not uncommonly, isorhythmic AV dissociation is seen in healthy young individuals, particularly when they are sleeping.

20. Ventricular Tachycardia
Monomorphic VT
Three or more successive ventricular beats are defined as ventricular tachycardia (VT). This VT is monomorphic since all of the QRS complexes have an identical appearance. Although the P waves are not distinct, they can be seen altering the QRS complex and ST-T waves in an irregular fashion, indicating the absence of a relationship between the P waves and the QRS complexes, ie AV dissociation is present.
The QRS complexes have markedly differing morphologies due to changes in the direction (vector) of myocardial activation.
Polymorphic VT

21. VT Treatments IV procainimide, amiodarone DC cardioversion
Severe, symptomatic VT
Implanted ICD
Indicated with decreased LV function
Radiofrequency ablation

22. Torsades de Pointes
“twisting of points” : changing axis of polymorphic QRS VT
Associated with congenital or acquired long QT, severe bradycardia, hypoK, hypoMg, meds (TCAs, procainimide, quinidine)
ECG findings
Wide QRS complexes of changing amplitudes that appear to twist about the isoelectric line
Ventricular rate bpm
Usually initiated by a long RR interval (like post PVC compensatory pause) followed by a short RR cycle ( e.g. R on T)
Treatment
Acquired: IV Magnesium + ventricular or atrial pacing
Congenital: B-blockers
Anti-arrhythmia drugs prolong the QT interval and worsen the arrhythmia
This is an atypical, rapid, and bizarre form of ventricular tachycardia that is characterized by a continuously changing axis of polymorphic QRS morphologies.
The electrocardiographic rhythm strip shows torsade de pointes, a polymorphic 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 the compensatory pause after the couplet.
Torsade de pointes — Torsade de pointes is an atypical, rapid, and bizarre form of ventricular tachycardia. It means "twisting of points," a name that refers to the continuously changing axis of polymorphic QRS morphologies that are observed during each episode (show ECG 12A-12B). The polymorphic ventricular tachycardia is associated with a congenital or acquired prolongation of the QT interval, suggesting a prolonged refractory period and repolarization time. There often is heterogeneity of repolarization or dispersion of refractoriness. Torsade is usually initiated by a long RR interval (often a post VPB compensatory pause) followed by a short RR cycle, generally due to another VPB (show ECG 12B). (See "Clinical features of congenital long QT syndrome")

23. Long QT syndrome Associated with Torsades and sudden death
Seen in young people whose ECG is normal except for long QT interval
Rhythm abnormality can be precipitated by a startle reaction
Two types
Jarvell-Lange-Neilson syndrome- deafness
Romano-Ward syndrome- without deafness
QTc >500ms in pts with LQT syndrome is associated with an increased risk of sudden death
QTc>430ms with FHx makes LQTS gene defect likely
A QTc of > 500ms in patients with Long QT Syndrome is associated with an increased risk for sudden death.[2]
In patients suspected of LQTS (e.g. family members of known LQTS patients) a QTc > 430ms makes it likely that a LQTS gene defect is present.[3]
Because the QTc can change with age, it is best to take the ECG with the longest QTc interval for risk stratification.[4]
"Lifestyle modification":
No competitive sports in all LQTS patients
No swimming in LQT1 patients
Avoid nightly noise in LQT2 patients (e.g. no alarm clock)
Medication: beta-blockers. Beta-blockers even reduce the risk of sudden death in patients in whom a genetic defect has been found, but no QT prolongation is visible on the ECG.
ICD implantation in combination with beta-blockers in LQTS patients with previous cardiac arrest or syncope or ventricular tachycardia while on beta-blockers.

24. Ventricular Fibrillation
Disordered ventricular impulses with no coordinated ventricular contraction
No cardiac output occurs & pt immediately loses consciousness
Can occur with any type of cardiac disease, electrolyte imbalance, hypoxemia, acidosis, shock, drugs (epi, cocaine)
ECG findings
Chaotic, irregular complexes; no discrete QRS waveforms
Rate: bpm
Can occur spontaneously or preceded by PVCs or VT
Treatment
Immediate defibrillation followed by anti-arrhythmic drugs to suppress further ventricular ectopy
There is a complete absence of properly formed QRS complexes and no obvious P waves. A recent onset (eg, within minutes) of the arrhythmia is suggested by the coarse morphology of the fibrillatory waves.
VENTRICULAR FIBRILLATION — Ventricular fibrillation is identified by the complete absence of properly formed QRS complexes and no obvious P waves (show ECG 14). There is no uniform activation of the ventricular myocardium and therefore no distinct ventricular complexes. There are coarse fibrillatory waves when the fibrillation is recent in onset (eg, only a few minutes); these are high amplitude oscillations occurring at rate greater than 320 beats per minute which manifest random changes in morphology, width, and height, leading to the appearance of a completely chaotic rhythm. The fibrillatory waves become fine when VF continues for a longer time and may not be obvious; they may resemble asystole in these cases.

25. Brugada syndrome Associated with VT/ VF and sudden death
If symptomatic, mortality risk up to 10% per yr
AD inheritance pattern, SCN5A gene mutation
Endemic in SE Asia
Arrhythmia start in 30-40’s, often during sleep or rest
May be triggered by fever, sodium channel blocker, or spontaneous
Approximately 20% of the cases of Brugada syndrome have been shown to be associated with mutation(s) in the gene that encodes for the sodium ion channel in the cell membranes of the muscle cells of the heart (the myocytes). The gene, named SCN5A, is located on the short arm of the third chromosome (3p21). Loss-of-function mutations in this gene lead to a loss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization. The transmural dispersion underlies ST-segment elevation and the development of a vulnerable window across the ventricular wall, whereas the epicardial dispersion of repolarization facilitates the development of phase 2 reentry, which generates a phase 2 reentrant extrasystole that captures the vulnerable window to precipitate ventricular tachycardia and/or fibrillation that often results in sudden cardiac death. At present time however, all the reported patients died because of the disease and submitted to detailed necropsy study, have shown a structural right ventricular pathology underlying the syndrome.
Over 160 mutations in the SCN5A gene have been discovered to date, each having varying mechanisms and effects on function, thereby explaining the varying degrees of penetration and expression of this disorder. [7]

26. ECG change in Brugada RV conduction delay or block morphology V1
In some cases, the disease can be detected by observing characteristic patterns on an electrocardiogram, which may be present all the time, or might be elicited by the administration of particular drugs (e.g., Class IC antiarrhythmic drugs that blocks sodium channels and causing appearance of ECG abnormalities - ajmaline, flecainide) or resurface spontaneously due to as yet unclarified triggers. The pattern seen on the ECG is persistent ST elevations in the electrocardiographic leadsV1-V3 with a right bundle branch block (RBBB) appearance with or without the terminal S waves in the lateral leads that are associated with a typical RBBB. A prolongation of the PR interval (a conduction disturbance in the heart) is also frequently seen.The electrocardiogram can fluctuate over time, depending on the autonomic balance and the administration of antiarrhythmic drugs. Adrenergic stimulation decreases the ST segment elevation, while vagal stimulation worsens it. (There is a case report of a patient who died while shaving, presumed due to the vagal stimulation of the carotid sinus massage) The administration of class Ia, Ic and III drugs increases the ST segment elevation, and also fever. Exercise decreases ST segment elevation in some patients but increases it in others (after exercise when the body temperature has risen). The changes in heart rate induced by atrial pacing are accompanied by changes in the degree of ST segment elevation. When the heart rate decreases, the ST segment elevation increases and when the heart rate increases the ST segment elevation decreases. However, the contrary can also be observed.
[edit] Treatment
The cause of death in Brugada syndrome is ventricular fibrillation.The episodes of syncope (fainting) and sudden death (aborted or not) are caused by fast polymorphic ventricular tachycardias or ventricular fibrillation. These arrhythmias appear with no warning. While there is no exact treatment modality that reliably and totally prevents ventricular fibrillation from occurring in this syndrome, treatment lies in termination of this lethal arrhythmia before it causes death. This is done via implantation of an implantable cardioverter-defibrillator (ICD), which continuously monitors the heart rhythm and will defibrillate an individual if ventricular fibrillation is noted. Some recently performed studies had evaluated the role of quinidine, a Class Ia antiarrhythmic drug, for decreasing VF episodes occurring in this syndrome. Quinidine was found to decrease number of VF episodes and correcting spontaneous ECG changes, possibly via inhibiting Ito channels.[9] Those with risk factors for coronary artery disease may require an angiogram before ICD implantation.
RV conduction delay or block morphology V1
Unusual ST elevation segments in V1-V3

27. Wide complex tachyarrhythmias
QRS greater or equal to 0.12 sec and rate >100 bpm
Not all are of ventricular origin
Differential
Ventricular tachycardia
Supraventricular tachycardia with aberrancy (conduction block) or presence of an accessory pathway with antegrade conduction (WPW syndrome)
Artifact

28. VT vs SVT with Aberrancy
Both manifest as wide complex tachycardias on ECG
Distinguishing ECG findings:
SVT with aberrant conduction
QRS > 0.14
Rhythm onset with premature P wave
PR interval <100msec
P wave and QRS are linked
Vagal maneuver slows/terminates rhythm
Monomorphic VT
QRS >0.14 msec
AV dissociation with fusion or capture beats
Absence of RS complex in precordial leads
Extreme axis deviation
If above findings fail to be detected, morphologic criteria used: if QRS in V1 does NOT look like typical R or L conduction block

29. VT vs SVT with Aberrancy

30. Clinical importance Misdiagnosing VT as SVT can lead to fatal error
Treating VT as SVT with verapamil, diltiazem, and adenosine can precipitate ventricular fibrillation, even if initially stable.
All wide complex tachyarrhythmia should be considered VT until proven otherwise

31. Take home points
PVCs are very common arrhythmias that can occur in healthy or diseased hearts with multiple features on ECG
VT and VF are dangerous arrhythmias that can lead to sudden cardiac death
Not all wide complex tachyarrhythmias arise from the ventricles
Distinguish between VT and SVT with aberrancy because the treatment and prognosis of each is very different

32. Reference Previous Harvey Hand out Up to date
ECG learning center
ECG pedia org
Lilly: Pathophysiology of Heart Disease. 3rd edition, 2003.
Google images