Cardiac Arrhythmias II: Tachyarrhythmias

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Cardiac Arrhythmias II Tachyarrhythmias

• Michael H. Lehmann, M.D.
• Clinical Professor of Internal Medicine
• Director, Electrocardiography Laboratory

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Supraventricular Tachycardias

• (Supraventricular - a rhythm process in which the
  ventricles are activated from the atria or AV
  node/His bundle region)

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Supraventricular Tachycardia (SVT)
Terminology

• QRS typically narrow (in absence of bundle
  branch block) thus, also termed narrow QRS
  tachycardia
• Usually paroxysmal, i.e, starting and stopping
  abruptly in which case, called PSVT
• Paroxysmal Atrial Tachycardia (PAT) - the older
  term for PSVT - is misleading and should be
  abandoned

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AV Junctional Reentrant Tachycardias (typically
incorporate AV nodal tissue)
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Mechanism of Reentry
Bidirectional Conduction
Unidirectional Block
Recovery of Excitability Reentry
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AV Nodal Reentrant Tachycardia
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AV Nodal Reentrant Tachycardia Circuit
F fast AV nodal pathway
S slow AV nodal pathway
(His Bundle)
During sinus rhythm, impulses conduct
preferentially via the fast pathway
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Initiation of AV Nodal Reentrant Tachycardia
PAC
PAC
PAC premature atrial complex (beat)
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Sustainment of AV Nodal Reentrant
Tachycardia
Rate 150-250 beats per min
P waves generated retrogradely (AV node ?
atria) and fall within or at tail of QRS
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Sustained AV Nodal Reentrant Tachycardia
V1
P
P
P
P
Note fixed, short RP interval mimicking r
deflection of QRS
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Orthodromic AV Reentrant Tachycardia
Anterogade conduction via normal pathway
AP
Retrograde conduction via accessory pathway (AP)
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Initiation of Orthodromic AV
ReentrantTachycardia
PAC
Atria
AP
AVN
Ventricles
PAC premature atrial complex (beat)
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Sustainment of Orthodromic AV Reciprocating
Tachycardia
Atria
Rate 150-250 beats per min
AP
AVN
Ventricles
Retrograde Ps fall in the ST segment with
fixed, short RP
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Accessory Pathway with Ventricular
Preexcitation (Wolff-Parkinson-White Syndrome)
Sinus beat
Hybrid QRS shape
Delta Wave
PR lt .12 s
AP
Fusion activation of the ventricles
QRS ? .12 s
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Varying Degrees of Ventricular
Preexcitation
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(No Transcript)
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Intermittent Accessory Pathway Conduction
V Preex
V Preex
Normal Conduction
Note all-or-none nature of AP conduction
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Orthodromic AV Reentrant Tachycardia
NSR with V Preex
Note retrograde P waves in the ST segment
SVT V Preex gone
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Concealed Accessory Pathway
Sinus beat
No Delta wave during NSR (but AP capable of
retrograde conduction)
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Summary of AV Junctional Reentrant Tachycardias

• Reentrant circuit incorporates AV nodal tissue
• P waves generated retrogradely over a fast
  pathway
• Short, fixed RP interval

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Clinical Significance of AV Junctional Reentrant
Tachycardias

• Rarely life-threatening
• However, may produce serious symptoms (dizziness
  or syncope fainting)
• Can be very disruptive to quality of life
• Involvement of an accessory pathway can carry
  extra risks

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Atrial Tachyarrhythmias
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Sinus Tachycardia (100 to 180 beats/min)

• P waves oriented normally
• PR usually shorter than at rest

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Causes of Sinus Tachycardia

• Hypovolemia ( blood loss, dehydration)
• Fever
• Respiratory distress
• Heart failure
• Hyperthyroidism
• Certain drugs (e.g., bronchodilators)
• Physiologic states (exercise, excitement, etc)

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Premature Atrial Complex (PAC)
V5
Non-Compensatory Pause
P
P
P
P
P
Timing of Expected P
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Premature Atrial Complex (PAC) Alternative
Terminology

• Premature atrial contraction
• Atrial extrasystole
• Atrial premature beat
• Atrial ectopic beat
• Atrial premature depolarization

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PACs Bigeminal Pattern
P
P
P
P
P
P

• Note deformation of T wave by the PAC
• Regularly Irregular Rhythm

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PACs with Conduction Delay/Block
Physiologic AV Block
P
P
Physiologic AV Delay
P
P
Recovered AV Conduction
P
P
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PAC with Aberrant
Conduction (Physiologic Delay in the His
Purkinje System)
V1
P
P
P
P
RBBB
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PACs with Aberrant Conduction (Physiologic RBBB
and LBBB)
V1
Normal conduction
RBBB
LBBB
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PACs with Physiologic LBBB and His-Purkinje
System Block
V1
Non-conducted PAC
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Non-Conducted PAC
V5
V1
P
P
P
P
Note deformation of T wave by the PAC
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Bigeminal/Blocked PACs Mimicking Sinus
Bradycardia
V1
Only the 4th bigeminal PAC conducts
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Clinical Significance PACs

• Common in the general population
• May be associated with heart disease
• Can be a precursor to atrial tachyarrhythmias

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Atrial Tachycardia
V1

• RP intervals can be variable
• RP often gt PR
• (Example slower than more common rate
  mof 150-250 beats per min)

Differs from AV nodal or AV reentrant SVT


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Clinical Significance of Atrial Tachycardia

• Similar to sequela of AV junctional reentrant
  tachycardias
• Must be differentiated from them diagnostically

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Atrial Flutter (Typical,
Counterclockwise)
Reentrant mechanism
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Atrial Flutter
Classic inverted sawtooth flutter waves at 300
min-1 (best seen in II, III and AVF)
II
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V1
Note variable ventricular response
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Atrial Flutter
V. rate 140-160 beats/min
21 Conduction (common)
21 32 Conduction
11 Conduction (rare but dangerous)
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Atrial Fibrillation
Focal firing or multiple wavelets
Chaotic, rapid atrial rate at 400-600 beats per
min
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Atrial Fibrillation
V5
V1

• Rapid, undulating baseline (best seen in V1)
• Most impulses block in AV node ? Erratic
  conduction

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Atrial Fibrillation Characteristic
Irregularly Irregular Ventricular Response
II
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Atrial Fibrillation with Rapid Ventricular
Response
II
Irregularity may be subtle
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Atrial Fibrillation Autonomic Modulation
of Ventricular Response
Baseline
Immediately after exercise
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Clinical Significance of Atrial Flutter and
Fibrillation

• Causes
• Usually occur in setting of heart disease
  but sometimes see lone atrial
  fibrillation
• Hyperthyroidism (atrial fibrillation)
• May acutely precipitate myocardial ischemia or
  heart failure
• Chronic uncontolled rates may induce
  cardiomyopathy and heart failure
• Both can predispose to thromboembolic stroke, etc

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Varying Degrees of Ventricular
Preexcitation
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Atrial Fibrillation with Rapid
Conduction Via Accessory Pathway
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Atrial Fibrillation with Third Degree AV Block
V1
V5
Regular ventricular rate reflects dissociated
slow junctional escape rhythm
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Regular Narrow QRS Tachycardias
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Differential Diagnosis of Regular Narrow QRS
(Supraventricular) Tachycardia

• Reentrant SVT incorporating AV nodal tissue
• AV nodal reentrant tachycardia
• Orthodromic AV reentrant tachycardia
• SVT mechanism confined to the atria
• Sinus tachycardia
• Atrial flutter
• Other regular atrial tachycardias
• Short-RP favors AV node-dependent reentrant SVT

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Determining AV Nodal Participation in SVT by
Transiently Depressing AV Nodal Conduction

• Vagotonic Maneuvers
• Carotid sinus massage
• Valsalva maneuver (bearing down)
• Facial ice pack (diving reflex for kids)
• Adenosine (6-12 mg I.V.)
• If SVT breaks, a reentrant mechanism involving
  the AV node is likely
• If atrial rate unchanged, but ventricular rate
  slows (Ps gt QRSs), SVT is atrial in origin

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SVT Responses to AV Nodal Depressant Maneuvers

• SVT termination
• AV nodal reentrant tachycardia
• Orthodromic AV reentrant tachycardia
• No SVT termination (despite maximal attempts)
• Sinus tachycardia
• Atrial flutter or fibrillation
• Most atrial tachycardias (a minority are
  adenosine-sensitive)

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Carotid Sinus Massage
Stimulation of carotid sinus triggers
baroreceptor reflex and increased vagal tone,
affecting SA and AV nodes
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Termination of SVT by Vagotonic
Maneuver (Carotid Sinus Massage)
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SVT
Carotid Sinus Massage
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SVT
Adenosine 6 mg
P
P
P
P
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Ventricular Tachyarrhythmias
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Premature Ventricular Complex (PVC)
Alternative Terminology

• Premature ventricular contraction
• Ventricular extrasystole
• Ventricular premature beat
• Ventricular ectopic beat
• Ventricular premature depolarization

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Premature Ventricular Complex (PVC)
Compensatory Pause
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(No Transcript)
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PVCs Bigeminal Pattern
Regularly Irregular Rhythm
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Accelerated Idioventricular Rhythm (?
Ventricular Escape Rate, but ? 100 bpm)
Fusion beat
Ectopic ventricular activation
Normal ventricular activation
Sinus acceleration
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AV Dissociation
ATRIA AND VENTRICLES ACT INDEPENDENTLY
SA Node
Ventricular Focus
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Ventricular Tachycardia (VT)
V1

• Rates range from 100-250 beats/min
• Non-sustained or sustained
• P waves often dissociated (as seen here)

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Ladder Diagram of AV Dissociation During
Ventricular Tachycardia


Slower atrial rate


Faster ventricular rate

Impulses invade the AV node retrogradely and
anterogradely, creating physiologic
interference and block. Under the right
conditions, some anterograde impulses may slip
through.
This phenomenon is not equivalent to third degree
AV block
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Ladder Diagram of AV Dissociation During
Third Degree AV Block
Faster atrial rate
Slower ventricular (escape) rhythm
Note that impulses block anterogradely and
retrogradely within the AV conduction system
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Monomorphic VT
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Polymorphic VT
V1
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Causes of PVCs and VT

• PVCs are fairly common in normals but are also
  seen in the setting of heart disease
• Monomorphic VT often implies heart disease, but
  can sometimes be seen in structurally normal
  hearts
• Polymorphic VT can result from myoardial ischemia
  or conditions that prolong ventricular
  repolarization
• Electrolyte derangements, hypoxemia and drug
  toxicity can cause PVCs and VT

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MI Scar-Related Sustained Monomorphic VT Circuit
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Torsade de
Pointes (Polymorphic VT Associated with
Prolonged Repolarization)
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Clinical Significance of PVCs and VT

• Can be a tip-off to underlying cardiac,
  respiratory or metabolic disorder
• VT may (but need not invariably) lead to
  hemodynamic collapse or more life-threatening
  ventricular tachyarrhythmias, increasing the risk
  of cardiac arrest

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Ventricular Flutter

• VT ? 250 beats/min, without clear isoelectric
  line
• Note sine wave-like appearance

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Ventricular Fibrillation (VF)

• Totally chaotic rapid ventricular rhythm
• Often precipitated by VT
• Fatal unless promptly terminated (DC shock)

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Sustained VT Degeneration to VF
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Atrial Fibrillation with Rapid Conduction Via
Accessory Pathway Degeneration to VF
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Diagnosing Regular Wide QRS Tachycardia
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Regular Wide QRS Tachycardia VT or SVT
with Aberrant Conduction?
V1
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Sustained Aberrant Conduction
V1
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Clinical Clues to Basis for Regular Wide QRS
Tachycardia

• REMEMBER VT does not invariably cause
  hemodynamic collapse patients may be conscious
  and stable
• History of heart disease, especially prior
  myocardial infarction, suggests VT
• Occurrence in a young patient with no known heart
  disease suggests SVT
• 12-lead EKG (if patient stable) should be obtained

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Regular Wide QRS Tachycardia VT or SVT
with Aberrant Conduction?
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More R-Waves Than P-Waves Implies VT!
II
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Artifact Mimicking Ventricular Tachycardia
QRS complexes march through the
pseudo-tachyarrhythmia
Artifact precedes VT