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  • Predictions about V:A time for DDX Circuits require two pathways with different conduction vel and different refractory periods
  • Tutorial of AF from PV
  • Anatomic barriers within the right atrium sustain the macro-reentry circuit. The AV node plays no part in the flutter circuit, so drugs aimed at altering the conduction of the AV node have no effect on the atrial rate.
  • Atrial flutter is distinguished from atrial tachycardia by the faster rate.
  • ECG characteristics of clockwise flutter are similar to those discussed in identifying counterclockwise flutter. A distinguishing difference is the pattern of the flutter waves. A “notched” upright pattern is often seen on the surface ECG inferior leads.
  • This slide shows a 12 lead ECG depicting clockwise flutter.
  • Atrial Flutter Atrial flutter is a form of reentry or circus tachycardia that utilizes the anatomy of the right atrium to sustain a loop of continuous depolarization. The loop is most typically counter-clockwise around the annulus of the tricuspid valve, following up the atrial septum and down the crista terminalis. Though the left atrium is depolarized, it is not part of the reentry circuit. Variable degrees of AV block may exist during atrial flutter (4 to 1 in this case) but this does not affect the flutter mechanism. On the ECG, note the saw-tooth shaped P wave, negative in leads II, III, and aVF, which indicates the retrograde conduction up the atrial septum, consistent with counter-clockwise flutter. [©2003 Blaufuss Multimedia. All rights reserved.]
  • Wolff-Parkinson-White syndrome: Initiation of SVT We’ve all seen how sinus rhythm fuses in the ventricle. An appropriately timed premature atrial beat may block in the AP and conduct to the ventricle solely over the normal AV conduction system. That takes some time b/c of AV nodal delay, and if that is a sufficient amount of time for the AP to recover, then it may conduct the impulse back to the atrium and begin an endless loop reentrant tachycardia. Conduction occurs over the AV conduction system to the ventricle, via ventricular myocardium to the AP, back to the atrium over the AP and back to the AV conduction system via atrial myocardium. When you consider the physiology that is operative, you discover that it is really a misnomer to call this a supraventricular tachycardia, because its mechanism is just as dependent on atrial myocardium to complete the circuit as it is on ventricular myocardium. Nonetheless, because the ventricle is activated over the normal AV conduction system, and hence, the QRS complex is narrow, it is considered a form of SVT. This type of SVT, the most common type of SVT that occurs in the WPW syndrome, is called AVRT. When the circuit travels to the ventricle over the normal AV conduction system, the circuit is traversed in an orthodromic direction. Of course, the reverse circuit can also occur, though it is much much less common. Antidromic tachycardia activates the ventricles solely over the AP and travels to the atrium retrogradely over the normal AV conduction system. For the remainder of the round, I will not consider antidromic AVRT any further b/c it is rare.
  • Welcome to VENTRICULAR TACHYARRHYTHMIAS – AN ELECTROPHYSIOLOGIC OVERVIEW . This module contains a discussion of the various characteristics and classifications of ventricular tachycardia (VT). ECG recognition and treatment of the various tachycardias will be explored. Focus is given to the use of RF ablation as a treatment for certain VTs.
  • VTs are generally classified as being either monomorphic or polymorphic. Detailed discussions of monomorphic VTs, (idiopathic, bundle branch, ventricular flutter,and ventricular fibrillation) will include a description of the rhythm, ECG characteristics, and treatment options.
  • Another characteristic, used to describe VT, is whether it is sustained or non-sustained.
  • PVC’s can lead to ventricular tachycardia or fibrillation in individuals with ischemic or damaged hearts. PVCs can occur in many combinations (e.g., bigeminal, trigeminal, couplets) or from many ectopic foci, (e.g., multifocal PVCs).
  • Ventricular tachycardia can be classified as being either monomorphic or polymorphic. The following slides present a discussion for each rhythm listed, along with EGC identification and treatment options. Ventricular flutter is rarely seen, and may be seen just prior to the onset of ventricular fibrillation. Torsades de pointes is associated with a long QT interval.
  • Monomorphic VT is regular, with uniform beat-to-beat morphology. It can be sustained, nonsustained, idiopathic or caused by bundle branch reentry.
  • ECG characteristics that help define VTs are: The QRS complexes are rapid, wide, and distorted. The T waves are large with deflections opposite the QRS complexes. The ventricular rhythm is usually regular. P waves are usually not visible. The PR interval is not measurable. A-V dissociation may be present. V-A conduction may or may not be present. It may be difficult to distinguish VT from SVT with aberrancy from a surface ECG. Many texts offer tips for distinguishing these rhythms. The presence of capture and fusion beats generally occur in VT.
  • This tachycardia may terminate with adenosine. It is catecholamine sensitive and usually inducible with isoproterenol.
  • This slide is a recording of RVOT VT.
  • Bundle branch reentry tachycardia is another VT that is treatable with RF ablation. With this type of tachycardia, the HV interval is increased. Ablation of the right bundle does cure this form of reentry. However, given the underlying LBBB, ablation of the RBBB results in either very impaired His/Purkinje function or in complete heart block. A pacer is usually required.
  • The most helpful criteria to consider when diagnosing VT due to bundle branch reentry is the comparison of this LBBB morphology to the LBBB seen in sinus. The morphology does not have to be exactly the same (if there is some conduction down the left bundle) but it should be really similar.
  • Rarely seen, ventricular flutter may occur just prior to the onset of ventricular fibrillation. It degenerates into ventricular fibrillation in a matter of seconds.
  • Ventricular fibrillation (VF) will convert to fine VF and then no electrical activity will be seen. Patients resuscitated from VF are deemed sudden cardiac death survivors.
  • The following ECG findings help electrophysiologists to diagnose VF: P waves and QRS complexes are not present. Heart rhythm is highly irregular. The heart rate is not defined (without QRS complexes).
  • A second classification of VT is polymorphic VT.
  • TdP is a rapid and distinct VT with a twisting configuration of the QRS morphology, associated with prolonged repolarization. It may be acquired or congenital. It is a very deadly form of VT.
  • The early afterdepolarizations initiate the tachycardia; reentry sustains it.
  • Torsades de pointes (twists of points) is a unique VT in which the QRS complexes change from positive to negative and appear to twist around the isoelectric line.
  • Possible causes of TdP can include drugs that lengthen the QT interval. Causes can also be physical in nature.
  • The treatment for TdP can be with drugs, overdrive pacing, or cardioversion. Of note, isoproterenol is contraindicated in patients with hypertension or ischemic heart disease. Treatment with potassium is dependent on the potassium blood level and is only given if the patient is hypokalemic. The treatment for congenital TdP is beta blockade and/or an ICD. The treatment for acquired TdP is avoiding pauses (acutely) and reversing the underlying cause.

Arrhythmias general Arrhythmias general Presentation Transcript

  • Arrhythmias
    • Ectopic Beats or Rhythms
    • beats or rhythms that originate in places other than the SA node
    • the ectopic focus may cause single beats or take over and pace the heart, dictating its entire rhythm
    • they may or may not be dangerous depending on how they affect the cardiac output
    Terminology and Basics
    • Causes of Ectopic Beats or Rhythms
    • hypoxic myocardium - chronic pulmonary disease, pulmonary embolus
    • ischemic myocardium - acute MI, expanding MI, angina
    • sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism
    • drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia, imbalances of calcium and magnesium
    • bradycardia - a slow HR predisposes one to arrhythmias
    • enlargement of the atria or ventricles producing stretch in pacemaker cells
    • Arrhythmia or Dysrhythmia?
    • dysrhythmia accurate, but arrhythmia most widely
    Terminology and Basics Supraventricular: origin is above the ventricle, i.e., SA, atrial muscle, AV or HIS origin Ventricular: origin is in ventricle Arrhythmia is generally named for anatomical site or chamber of origin
    • Automaticity: Spontaneous Phase 4 Depolarization (SA, AV, Purkinje tissue)
    • rate dependent on:
      • Threshold potential
      • slope of phase 4 depolarization
      • resting membrane potential
    • Mechanisms of Arrhythmias
    • Altered automaticity
      • Normal, enhanced normal, abnormal
    • Triggered activity
    • Reentry
    Mechanisms
  • 2. Triggered Activity
    • Afterdepolarization reaches threshold
      • Early: interrupt repolarization
        • Congenital or acquired long QT syndrome: altered K + and Na + currents during phase 2 can produce dangerous V-tach
      • Delayed: after completion of AP.
    3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)
    • Anatomic: nodal tissue, Purkinje, BB, accessory path
      • Example: WPW
    • Functional
      • Local differences in conduction velocity and membrane characteristics
    • Anisotropic:
      • circuit determined by difference in conduction velocity through length of fiber
    • Reflection
      • Parallel pathways with depressed segments
  • 3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)
    • Requires: available circuit, unidirectional block, and different conduction speed in limbs of circuit
      • Conditions that depress conduction velocity or shorten refractory period promote functional block
      • Exp: WPW reciprocating tachycardia, AV-nodal reentry, V-tach due to bundle branch reentry, infarcted area.
  • Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery The “Re-Entry” Mechanism of Ectopic Beats & Rhythms Electrical Impulse Cardiac Conduction Tissue
    • Tissues with these type of circuits may exist:
      • in microscopic size in the SA node, AV node, or any type of heart tissue
      • in a “macroscopic” structure such as an accessory pathway in WPW
  • Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Premature Beat Impulse Cardiac Conduction Tissue
        • 1. An arrhythmia is triggered by a premature beat
        • 2. The beat cannot gain entry into the fast conducting pathway because of its long refractory period and therefore travels down the slow conducting pathway only
    Repolarizing Tissue (long refractory period) The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
        • 3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
    Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
        • 4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit
    Fast Conduction Path Slow Recovery Slow Conduction Path Fast Recovery Cardiac Conduction Tissue The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
    • Atrial Re-entry
    • atrial tachycardia
    • atrial fibrillation
    • atrial flutter
    • Atrio-Ventricular Re-entry
    • Wolf Parkinson White
    • supraventricular tachycardia
    • Ventricular Re-entry
    • ventricular tachycardia
    • Atrio-Ventricular Nodal Re-entry
    • supraventricular tachycardia
    Re-entry Circuits as Ectopic Foci and Arrhythmia Generators
    • Clinical Manifestations of Arrhythmias
    • many go unnoticed and produce no symptoms
    • palpitations – ranging from “noticing” or “being aware” of ones heart beat to a sensation of the heart “beating out of the chest”
    • if Q is affected (HR > 300) – lightheadedness and syncope, fainting
    • drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia, imbalances of calcium and magnesium
    • very rapid arrhythmias u myocardial oxygen demand r ischemia and angina
    • sudden death – especially in the case of an acute MI
    • mechanism differentiation from ECG very difficult to impossible
    • Clinical Application
    • No rhythms precisely regular
    • Incidence: common (PVC, PAC), increase with age
    • ECG differentiation may be impossible
      • Monitor leads V 1 or MCL 1 : L&R ventricular ectopy, RBBB & LBBB, good P-waves
      • Where to look for clues
        • P-wave morphology
        • PR interval
        • QRS morphology
        • QTc interval
        • Matching atrial rate with ventricular
        • Look for gaps in the rhythm
    • Clinical Application
    • Eight basic rhythm disturbances
      • early beats (extrasystole)
      • unexpected pauses (nonconducted atrial extrasystole)
      • bradycardia (sinus bradycardia)
      • tachycardia (ventricular or atrial)
      • bigeminal rhythm (ventricular or supraventricular extrasystolic)
      • group beating (2 nd degree heart block)
      • total irregularity (atrial fibrillation)
      • regular non-sinus rhythm at normal rate (accelerated AV rhythm)
  • Abnormal rhythm
    • It can be one of the two extreme forms –
    • Tachyarrhythmia –a) supraventricular
    • b) Ventricular origin
    • Bradyarrhythmia
  • Supraventricular Tachycardia- Classification Atrial Flutter Atrial fibrillation Junctional Junctional ectopic tachycardia Atrial Tachycardia Unifocal Multifocal AVRT Concealed accessory pathway Wolf-Parkinson –White syndrome Sinus tachycardia Physiologic Inappropriate Sinus node re-entry AVNRT Typical( ‘common’, slow –fast) Atypical( ‘uncommon’, Fast-slow) AV node Independent (atrial) tachycardias AV node dependant tachycardias
  • SUMMARY Mechanisms of SVT Atrial Tachycardia AVNRT AVRT FP SP
  • Sinus Rhythm
    • Originates in sinus node
    • Innervated from right sided sympathetic and parasympathetic trunks
    • Parasympathetic (i.e. vagal tone) predominates
    • Normal range is 60 to 100 bpm with gradual changes in rate
    • Sinus “p waves” are upright (+) in lead II
  • Sinus rhythm
    • It is characterized by P waves of sinus origin, constant and normal PR interval, and constant P wave configuration in a lead with rate between 60-80 / minute and rhythm under the influence of autonomic system
  • Normal sinus rhythm Rate of 78 bpm Sinus p wave
  • Sinus Arrhythmia
    • Phasic (respiratory) sinus arrhythmia is characterized by an ac­celeration of the heart rate with inspiration and slowing with expiration.
    • Electrocardiographic features
    • 1.A variation of at least 0.12 s between the longest and shortest PP intervals, with normal and constant P-wave configu­ration.
    • 2.Maximum cycle length minus minimum cycle length divided by minimum cycle length is > 10%
  • Sinus Tachycardia >100b/min 1. Normal P waves 2. Normal or shortened PR interval 3. QRS and T vectors are normal 4. ST segments are normal 5. RR interval short <15mm 1500/100 = 15 Fig 3 Normal sinus rhythm Sinus tachycardia Sinus bradycardia
  • Sinus Bradycardia <60b/min 1. P waves are present and all are followed by a QRS 2. Normal and constant PR interval 3. QRS and T vectors are normal 4. ST segments are normal 5. RR interval long >25mm 1500/60 = 25 Fig 3 Normal sinus rhythm Sinus tachycardia Sinus bradycardia
  • Premature atrial contraction (PAC) 1. Arises from an ectopic focus in the atria. 2. Will have an identifiable P wave but the shape of the P wave may be altered 3. May have a normal QRS 4. May have a compensatory pause
  • The QRS may be altered if some of the ventricle is still in its refractory period. The compensatory pause is lacking because the SA node was reset. The rhythm has been shifted.
    • Primarily concerned with SVT – supraventricular tachycardia
    • Ectopic Atrial Tachycardia
    • Atrial fibrillation and flutter
    • Atrioventricular Nodal Reentry (AVNRT)
    • SVT associated with the Wolff-Parkinson-White Syndrome (AVRT)
    Supraventricular Rhythms
  • Atrial Tachycardia
    • Ectopic atrial focus
      • Reentrant, automatic or triggered
    • 150-250 bpm
    • 1:1 AV conduction
    • Paroxysmal or “warm up”
    • P wave morphology variable
  • Focal Atrial Tachycardia CSO IVC RAFW RAA LAA LAFW PV SN I A S CT * * * SVC
  • 20 yr woman with post-partum congestive heart failure I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
  • Specific Diagnostic Evaluation Ectopic atrial focus
    • Since the rhythm is initiated by enhanced automaticity of a single focus, the first ectopic and the subsequent P-wave morphology are identical.
    • The rate at onset varies and gradually accelerates as the focus &quot;warms up.&quot;
    • AV nodal block may exist.
    • Vagal maneuvers do not terminate the rhythm, although they may produce AV block and thus, reduce heart rate
    • The PR interval is related to the rate of tachycardia.
    • The vector of the ectopic P wave is usually normal with upright P waves in leads II, III, and aVF, although the P wave appear slightly different from the normal P wave.
    Specific Diagnostic Evaluation
  • Atrial tachycardia
  • Multifocal Atrial Tachycardia
    • The rate is usually 100 to 150/min with at least three P waves of at least three different morphologies identified in a single lead. The atrial rate is slightly irregular, and the PR interval also varies.
  • MAT
  • Atrial fibrillation and flutter
    • Over 2.2 million Americans have atrial fibrillation
    • Prevalence in the general population is 0.4%
    • Prevalence increases with age, rising to over 8% in people 80 years or older
    Atrial Fibrillation
  • Introduction…
    • AF is characterised by wavelets propagating in different directions causing disorganized atrial depolarization without effective atrial contraction
    • Electrical activity of atrium can be detected in ECG as small irregular baseline undulations of variable amplitude & morphology (f waves) at rate of 350 to 600
    • Ventricular response is irregularly irregular, & in untreated patients with normal AV conduction, is usually between 100 to 160
  • Atrial fibrillation 1. Irregularly irregular 2. No P waves
  • Underlying causes of AF
    • CVS
    • Rheumatic heart disease
    • ASD
    • Cardiac surgery
    • Cardiomyopathy
    • Hypertrophic
    • Idiopathic
    • Infiltrative
    • Hypertension
    • CAD (Acute & chronic)
    • MVPS
    • Non rheumatic mitral or tricuspid valve disease
    • Pericarditis
    • Tacycardia-bradycardia syndrome
    • Tumors
    • WPW syndrome
    • Systemic
    • Alcohol (holiday heart syndrome)
    • CVA
    • COPD
    • Defibrillation
    • Effort
    • Electrocution
    • Electrolyte abnormalities
    • Fever
    • Hypothermia
    • Pneumonia
    • Pulmonary embolism
    • Sudden emotion
    • Thyrotoxicosis
    • Trauma
    • Rare
    • Acute hypovolemia
    • Congenital
    • Multiple sclerosis
    • Muscular dystrophy
    • Pheochromocytoma
    • Right atrial cold injections
    • Swallowing
    • Tyramine foods
    Underlying causes of AF…
  • Mechanism is activation of multiple wavelets within the right and left atrium Recent studies have shown pulmonary vein foci trigger some episodes Atrial Fibrillation
  • Mechanisms
  • Atrial fibrillation AF originating in LSPV
  • Atrial Fibrillation Clinical Classification
    • Paroxysmal
    • Persistent
    • Permanent
  • Introduction
    • Paroxysmal AF
    • Short lasting < 1 hour
    • Long lasting >1; < 48 hours
    • AF interspersed with periods of sinus rhythm & usually terminates spontaneously
    • Persistent AF
    • Occur between 2days - weeks
    • Intervention is needed to restore the sinus rythum
    • Chronic or permanent AF
    • Persists for months to years
    • No spontaneous conversion
    • Interventions to restore sinus rythum are either ineffectual or not tried
  •  
  • Atrial Fibrillation
    • Atrial Fibrillation ECG:
    • 1) .Absence of P waves 2) .P waves replaced by f waves. 3) .f waves : irregular in size ,shape ,and spacing. Rate between 350 and 600 4) . Irregularly irregular ventricular rhythm, best seen in Ⅱ , Ⅲ ,Avf,V 1 or V 2.
  • No clear p waves Variable RR intervals Atrial Fibrillation
    • Type – I --- Activation consisted of single, broad wavefronts propagating without conduction delay & either only short arcs of conduction block or small areas of slow conduction that did not disrupt the main course of propagation
    • Type – II --- Activation consisted of either the presence of 2 wavelets or of single wave (with either considerable conduction block or slow conduction or both)
    • Type – III --- Activation was characterized by 3 or more wavelets combined with areas of slow conduction & multiple arcs of conduction block
    • As the fibrillation changed from type I to III, AFs frequency & irregularity increased, creating a higher incidence of continuous electrical activity & reentry
    Mechanisms
  • Classification of AF
  • Atrial Fibrillation with Apparent regularity of RR interval
    • A Fib with CHB
      • Degenerative AV block
      • Dig Toxicity
      • End stage Sick Sinus Syndrome
    • Afib at very fast heart rates
  • “ Typical isthmus dependent atrial flutter” is due to a macro reentrant circuit around the tricuspid valve
    • This rhythm can be stopped by pacing and cured with ablation
    • Embolic risk may be less than in fibrillation, but same recommendations apply
    Atrial Flutter
  • Ventricular rate 150 bpm “ Saw tooth” p waves Atrial Flutter
  • Reentry Circuit of Common Atrial Flutter Morady F. N Engl J of Med. 1999;340:534-544.
  • ECG Recognition counterclockwise flutter
    • Counterclockwise atrial flutter
      • Atrial rate: 240 - 340 bpm
      • Rhythm: Regular
      • Ventricular rate: Variable
        • Dependent upon:
          • AV node conduction properties
          • Usually a 2:1, 4:1 fixed conduction ratio
      • Recognition: “Sawtooth” appearance on the surface ECG
  • ECG Recognition counterclockwise flutter
  • ECG Recognition – Clockwise flutter
    • Clockwise atrial flutter
      • Atrial rate: 240 - 340 bpm
      • Atrial rhythm: Regular
      • Ventricular rate: Variable
        • Dependent upon:
          • AV node conduction properties
          • Usually a 2:1, 4:1 fixed conduction ratio
      • Recognition: “notched” upright pattern on the inferior surface ECG
  • ECG Recognition – Clockwise flutter ECG used with permission of Dr. Brian Olshansky.
    • Counterclockwise right atrial reentry
    • LA is passively activated
    Atrial Flutter
  • Atrial Flutter Ablation in cavo-tricuspid isthmus (CTI)
  • Atrioventricular Nodal Reentrant Tachycardia (AV Node Reentry or AVNRT)
    • Most common cause of paroxysmal SVT in the young adult
    • Occurs over a small reentrant circuit located near the AV node
    • The circuit consists of a fast and slow pathway connected by a common top and bottom pathway
  • Supraventricular Tachycardia Due to AV Nodal Reentry(AVNRT)
    • This supraventricular tachycardia with a regular ventricular rate varying between 160 to 260 beats per minute is due to AV nodal reentry.
  • Mechanism- Dual pathway physiology in AV node
  • Specific Diagnostic Evaluation
    • Examination of a 12-lead electrocardiogram may reveal a retrograde P wave buried in the QRS complex or immediately following the QRS complex,
    • P waves may fall on terminal part of S wave in V1, so as to produce pseudo R’ wave in V1
    • P waves may fall in terminal part of R waves in lead II, so as to produce a pseudo S wave
    • The PAC initiating AV nodal tachycardia has a long PR interval as a result of antegrade conduction down the slow-conducting alpha pathway.
    • The rhythm may be initiated and terminated by a PAC or PVC.
    • Vagal maneuvers may slow and then abruptly terminate the rhythm
  • AVNRT
  • Adenosine conversion of AVNRT to SR
  • AV Node Reentry Tachycardia Rate of 145 bpm (Short RP tachycardia) RP = 60 msec Retrograde p waves
  • Wolff-Parkinson-White Syndrome
    • Relatively common cause of paroxysmal SVT in children and young adults
    • Due to an “extra” muscular bridge that connects the atrium and ventricle and allows the ventricle to be “excited” before the signal passing through the AV Node
  • Wolff-Parkinson-White Syndrome
  • Preexcitation
    • Preexcitation exists when, in relation to atrial events, all or part of the ventricular muscle is activated by an impulse over an accessory (bypass) pathway sooner than the impulse arriving by way of the normal AV system.
  • Specific Diagnostic Evaluation
    • 12 lead ECG during SR
    • • Short PR interval (less than 0.12 s]
    • • Normal P-wave vector.
    • • QRS duration greater than 0.10 s. A 12-lead electrocardiogram during atrial fibrillation or atrial flutter may reveal delta waves.
  •  
  • Wolf-Parkinson-White (WPW) Syndrome (Right sided pathway) Rate = 62 bpm QRS is wide (over 120 msec) PR interval is short (80 to 90 msec)
  • Wolf-Parkinson-White (WPW) Syndrome (Left sided pathway) Rate = 100 bpm QRS is wide (over 120 msec) PR interval is short (80 to 90 msec)
  • Types of accessory pathways
    • Based on site of origin and insertion
    • a.Atrioventricular( Kent fibres)
    • i. Right sided: anteroseptal , RV free wall, posteroseptal
    • ii.Left sided: anteroseptal , LV free wall, posteroseptal
    • b. Atriofsicular (Brechenmacher fibres)
    • c. Nodofacicular fibres( Mahaim)
  • Types of accessory pathways
    • II. Based on direction of conduction
        • Antegrade
        • Retrograde( concealed)
        • Bidrectional
    • III. Based on conduction property
    • Slow, decremental
    • Fast, non decremental
    • IV. Based on numbers
    • Single
    • Multiple
  • Types of conduction over accessory pathway
  • Types of conduction over accessory pathway Orthodromic conduction: A premature impulse (APC, VPC) conducts antegradely through AV node, retrogradely through accessory pathway Antidromic conduction : Impulse conducts antegradely over accessory pathway and retrogradely over AV node
  • Wolff-Parkinson-White Syndrome Tachycardias
  • WPW: Initiation of SVT Supraventricular tachycardia • initiated by a closely coupled premature atrial complex (PAC) • blocks in the accessory pathway • but conducts through the AV node • retrograde conduction via accessory pathway • inverted P wave produced by retrograde conduction visible in the inferior ECG leads
  • AV reentrant tachycardia ( AVRT)
    • often reveal a negative P wave in lead-I. The RP interval is usually less than one-half the RR interval.
    • The rhythm may be initiated and terminated by a PAC or a PVC.
    • Vagal maneuvers sometimes slow and abruptly terminate the rhythm.
    • QRS alternance can be seen in few cases
    • Prolongation of tachycardia cycle length associated with bundle branch block usually localizes the accessory pathway to the side of bundle branch block
  • AVRT- note short RP interval, well seen P waves, an example of orthodromic conduction
  • Atrial fibrillation with antegrade conduction over accessory pathway
    • Asymptomatic patient - no further evaluation or treatment is required
    • Some “high risk” occupations - such as airline pilots - may require further evaluation even if they are asymptomatic
    • Some physicians will advocate exercise treadmill testing or the induction of atrial fibrillation to access the patients risk of SCD even if the patient is asymptomatic.
    Wolf-Parkinson-White (WPW) Syndrome
  • Wolf-Parkinson-White (WPW) Syndrome
    • Symptomatic patients - first step is correlating the patient’s symptoms with SVT. This is especially true if the patient complains of “palpitations”. If syncope or SCD has occurred, however, most would proceed to EPS.
    • After the presence of SVT has been established, most cardiologists would recommend diagnostic electrophysiology study (EPS) to characterize the accessory pathway.
    • Treatment can be best defined by EP study
    • If the patient with WPW can conduct rapidly down the accessory pathway, it is possible that the patient could have ventricular fibrillation and SCD by rapidly conducting the atrial impulses down the pathway
    • The administration of AV nodal blocking agents can increase the risk of this rapid conduction
    • If a patient with WPW demonstrates consecutive preexcited (i.e. wide) QRS complexes during atrial fibrillation that are less than 250 msec apart, they are at increased risk for SCD.
    Atrial fibrillation can coexist with WPW.
  • Dr Dattatreya Ventricular Tachyarrhythmias
  • Ventricular Tachyarrhythmias
    • Classification
      • VPC
      • 1. Unifocal
      • 2. Multi focal
      • 3. Monomorphic
      • 4. Poly morphic
      • Ventricular tachycardia
      • 1. NSVT
      • 2. Sustained VT
  • 3.Mnomorphic VT 4. Polymorphic VT C. Ventricular flutter D. Ventricular fibrillation
  • actually a &quot;retrograde p-wave may sometimes be seen on the right hand side of beats that originate in the ventricles, indicating that depolarization has spread back up through the atria from the ventricles QRS is wide and much different (&quot;bizarre&quot;) looking than the normal beats. This indicates that the beat originated somewhere in the ventricles and consequently, conduction through the ventricles did not take place through normal pathways. It is therefore called a “ventricular” beat Ventricular Escape Beat there is no p wave, indicating that the beat did not originate anywhere in the atria Ventricular Beats & Rhythms
    • Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles) :
    • A ventricular ectopic focus discharges causing an early beat
    • Ectopic beat has no P-wave (maybe retrograde), and QRS complex is &quot;wide and bizarre&quot;
    • QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant)
    • In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion
    • PVC’s are sometimes described by lay people as “skipped heart beats”, often normal variant
    Ventricular Beats & Rhythms
    • Characteristics of PVC's
    • PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)
    • T-waves for PVC’s are usually large and opposite in polarity to terminal QRS
    • Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle
    • Every other beat being a PVC (bigeminy) may indicate coronary artery disease
    • Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s
    Interpolated PVC – note the sinus rhythm is undisturbed The classic PVC – note the compensatory pause Ventricular Beats & Rhythms
  • Premature Ventricular Complex (PVC) - Summary ECG Patterns Rate: can occur at any rate and with any rhythm Rhythm: normally irregular due to pause after PVC P wave: normally none associated with PVC; may be retrograde P-R: none evident QRS: usually wide (>.11s) and bizarre with T directed opposite QRS deflection; BBB configuration; different from flanking beats Comment: usually followed by fully compensatory pause; usually don't generate a peripheral pulse
    • PVC Summary (cont)
    • Post extrasystolic cycle may be less than compensatory when:
      • retrograde conduction to atria disturbs SA
      • Post extrasystolic cycle ends with escape beat
      • interpolated PVC
    • Mechanism
      • Ectopic focus or reentry???
    • Morphology of PVC's
      • left vs right PVC's - best recognized in V 1
      • '+' in V 1 => LV origin; called RBBB pattern
          • usually monophasic R or qR in V 1
          • rS or QS in V 6
          • left rabbit ear taller than right in V 1 ; often opposite if true RBBB
        • ‘ -” in V 1 => RV origin, LBBB pattern
        • importance
          • LV more likely with HD
          • LV more likely to precipitate V-tach in acute MI
    • PVC's are Dangerous When :
    • They are frequent (> 30% of complexes) or are increasing in frequency
    • The come close to or on top of a preceding T-wave (R on T)
    • Three or more PVC's in a row (run of V-tach)
    • Any PVC in the setting of an acute MI
    • PVC's come from different foci (&quot;multifocal&quot; or &quot;multiformed&quot;)
    • These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:
    • Ventricular Tachycardia
    • Ventricular Fibrillation
    sinus beats Unconverted V-tach r V-fib V-tach “ R on T phenomenon” time The sooner defibrillation takes place, the increased likelihood of survival Ventricular Beats & Rhythms
    • Notes on V-tach :
    • Causes of V-tach
      • Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause)
    • Typical V-tach patient
      • MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm)
    • V-tach complexes are likely to be similar and the rhythm regular
      • Irregular V-Tach rhythms may be due to to:
        • breakthrough of atrial conduction
          • atria may “capture” the entire beat beat
          • an atrial beat may “merge” with an ectopic ventricular beat (fusion beat)
    Fusion beat - note p-wave in front of PVC and the PVC is narrower than the other PVC’s – this indicates the beat is a product of both the sinus node and an ectopic ventricular focus Capture beat - note that the complex is narrow enough to suggest normal ventricular conduction. This indicates that an atrial impulse has made it through and conduction through the ventricles is relatively normal. Ventricular Beats & Rhythms
    • Ventricular Tachycardia (VT)
        • Rate: 140-220 (200±50); at least 3 ectopic QRS in row
        • Rhythm: generally regular (may be slightly irregular)
        • P wave: no related P waves
        • P-R: none
        • QRS: normally wide and bizarre; (  0.14 sec favors VT)
    • Usually associated with MI or other organic HD; unusual in normals
    • Often serious requiring quick treatment if sustained
    • Mechanism? Reentry or rapid firing ectopic??
    • ECG diagnosis - clues to rule in VT
    • Difficult to rule out SVT with aberrant ventricular conduction
      • use more leads whenever possible - MCL 1 or V 1
    • Unrelated P's (independent atrial activity) - rules out atria
    • Presence of fusion beats suggests VT as contrasted to SVT
    • LVT favored - monophasic pattern in R chest leads (V1 or MCL1) with taller left 'rabbit ear‘
    • Concordant positivity (all complexes positive) in V leads => favors LV ectopy (rule out WPW)
    • concordant negativity = favors RV ectopy (rule out LBBB)
    • QRS interval > .14 sec (prior tracing available to rule out BBB)
  • Sustained vs. Nonsustained
    • Sustained VT
      • Episodes last at least 30 seconds
      • Commonly seen in adults with prior:
        • Myocardial infarction
        • Chronic coronary artery disease
        • Dilated cardiomyopathy
    • Non-sustained VT
      • Episodes last at least 6 beats but < 30 seconds
  • Premature Ventricular Contraction
    • PVC
      • Ectopic beat in the ventricle that can occur singly or in clusters
      • Caused by electrical irritability
    • Factors influencing electrical irritability
      • Ischemia
      • Electrolyte imbalances
      • Drug intoxication
  • Classification
    • Ventricular Tachycardia
      • Monomorphic
        • Idiopathic VT
        • Bundle branch reentry tachycardia
        • Ventricular flutter
        • Ventricular fibrillation
      • Polymorphic
        • Torsades de pointes (TdP)
  • Monomorphic VTs
  • Monomorphic VT
    • Heart rate: 100 bpm or greater
    • Rhythm: Regular
    • Mechanism
      • Reentry
      • Abnormal automaticity
      • Triggered activity
    • Recognition
      • Broad QRS
      • Stable and uniform beat-to-beat appearance
  • ECG Recognition ECG used with permission of Dr. Brian Olshansky.
  • Idiopathic Right Ventricular Tachycardia
    • Right ventricular idiopathic VT
      • Focus originates within the right ventricular outflow tract
      • Ventricular function is usually normal
      • Usually LBBB, inferior axis
    • Treatment options:
      • Pharmacologic therapy (beta blockers, verapamil)
      • RF ablation
  • ECG Recognition Kay NG. Am J Med 1996; 100: 344-356.
  • Bundle Branch Reentry
    • Reentry circuit is confined to the left and right bundle branches
    • Usually LBBB, during sinus rhythm
    • Presents with:
      • Syncope
      • Palpitations
      • Sudden cardiac death
    • Treatment: RF ablation of right bundle
  • VT Due to Bundle Branch Reentry
  • Ventricular Flutter
    • Heart rate: 300 bpm
    • Rhythm: Regular and uniform
    • Mechanism: Reentry
    • Recognition:
      • No isoelectric interval
      • No visible T wave
      • Degenerates to ventricular fibrillation
    • Treatment: Cardioversion
  • Ventricular Fibrillation
    • Heart rate: Chaotic, random and asynchronous
    • Rhythm: Irregular
    • Mechanism: Multiple wavelets of reentry
    • Recognition:
      • No discrete QRS complexes
    • Treatment:
      • Defibrillation
  • ECG Recognition
    • P waves and QRS complexes not present
    • Heart rhythm highly irregular
    • Heart rate not defined
  • Polymorphic VT
  • Polymorphic VT
    • Heart rate: Variable
    • Rhythm: Irregular
    • Mechanism:
      • Reentry
      • Triggered activity
    • Recognition:
      • Wide QRS with phasic variation
      • Torsades de pointes
  • ECG Recognition EGM used with permission of Texas Cardiac Arrhythmia, P.A.
  • Torsades de Pointes (TdP)
    • Heart rate: 200 - 250 bpm
    • Rhythm: Irregular
    • Recognition:
      • Long QT interval
      • Wide QRS
      • Continuously changing QRS morphology
  • Mechanism
    • Events leading to TdP are:
      • Hypokalemia
      • Prolongation of the action potential duration
      • Early afterdepolarizations
      • Critically slow conduction that contributes to reentry
  • ECG Recognition
    • QRS morphology continuously changes
    • Complexes alternates from positive to negative
  • Possible Causes
    • Drugs that lengthen the QT:
      • Quinidine
      • Procainamide
      • Sotalol
      • Ibutilide
    • Physical
      • Ischemia
      • Electrolyte abnormalities
  • Treatment
    • Pharmacologic therapy:
      • Potassium
      • Magnesium
      • Isoproterenol
      • Possibly class Ib drugs (lidocaine) to decrease refractoriness/shorten length of action potential
    • Overdrive ventricular pacing
    • Cardioversion
  • Wide ComplexTachycardias
    • Ventricular Tachycardia
    • SVT with aberrancy (functional bundle branch block)
    • SVT with underlying bundle branch block
    • SVT with pre-excitation
  • Additional Mimimics of Wide Complex Tachycardias
    • SVT with severe hyperkalemia
    • SVT with use of antiarrhythmic agents particularly 1C agents
    • SVT with acute MI
  • Wide-Complex Tachycardia
    • Majority are sinus tachycardia with bundle branch block
    • In higher risk population , previous MI, Decreased Left ventricular dysfunction
      • Predominantly Ventricular Tachycardia
  • Differentiating Ventricular Tachycardia from SVT with Aberrancy
    • Leads to correct initial therapy
    • Avoids use of Verapamil which may precipitate hemodynamic collapse with V.T.
    • Cannot use rate or the presence or absence of symptoms as discriminator !
    • Use ECG criteria for diagnosis
    • Use presence of risk factors for V.T. as discriminator
  • Electrocardiographic Differentiation of VT vs. SVT with Aberrancy
    • Clinical history – if the patient has had an MI in the past?…it is VT until proven otherwise
    • AV dissociation
    • QRS morphology
    • QRS axis
    • Fusion beat
    • Capture beat
  • A-V Dissociation, Fusion, and Capture Beats in VT Fisch C. Electrocardiography of Arrhythmias. 1990;134. ECTOPY FUSION CAPTURE V1 E F C
  • ECG Distinction of VT from SVT with Aberrancy
    • Favors VT Favors SVT with Aberrancy
    Duration RBBB: QRS > 0.14 sec. < 0.14 sec. LBBB: QRS > 0.16 sec. < 0.16 sec. Axis QRS axis -90° to ±180° Normal
  • ECG Distinction of VT from SVT with Aberrancy
    • Favors VT Favors SVT with Aberrancy
    Morphology Precordial concordance If LBBB: V 1 duration > 30 ms S wave > 70 ms S wave notched or slurred V 6 : qR or QR R wave If RBBB: V 1 : monophasic R wave qR If triphasic, R > R 1 R < R 1 V 6 : R < S
  • The Brugada Criteria
  • Morphology Criteria for VT
  • Therapy for Ventricular Tachycardia
    • Clinical condition of patient
      • Unstable requires DC cardioversion
      • Stable may be treated with Drugs or Cardioversion
    • Presence or absence of Left ventricular Dysfunction determines choice of pharmacologic therapy
      • Amiodarone 150 mg I.V. over 10 minutes may be RX of choice maximum 2.2 gm/24 hours class IIA recommendation