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Cardiac Arrhythmias II : Tachyarrhythmias Michael H. Lehmann, M.D. Clinical Professor of Internal Medicine Director, Electrocardiography Laboratory Supraventricular Tachycardias

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Cardiac arrhythmias ii tachyarrhythmias l.jpg
Cardiac Arrhythmias II: Tachyarrhythmias

Michael H. Lehmann, M.D.

Clinical Professor of Internal Medicine

Director, Electrocardiography Laboratory


Supraventricular tachycardias l.jpg
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 Circuit

F = fastAV

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 P’s 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 < .12 s

AP

Fusion activation

of the ventricles

QRS  .12 s


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Varying Degrees of

Ventricular Preexcitation


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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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Sinus Tachycardia (100 to 180 Tachycardias+ beats/min)

  • P waves oriented normally

  • PR usually shorter than at rest


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Causes of Sinus Tachycardia Tachycardias

  • 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) Tachycardias

V5

Non-Compensatory

Pause

P

P

P

P’

P

Timing of

Expected P


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Premature Atrial Complex (PAC): Tachycardias Alternative Terminology

  • Premature atrial contraction

  • Atrial extrasystole

  • Atrial premature beat

  • Atrial ectopic beat

  • Atrial prematuredepolarization


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PACs: Bigeminal Pattern Tachycardias

P

P’

P

P’

P

P’

  • Note deformation of T wave by the PAC

  • “RegularlyIrregular” Rhythm


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PACs with Conduction Delay/Block Tachycardias

Physiologic

AV Block

P

P’

Physiologic

AV Delay

P

P’

Recovered

AV Conduction

P

P’


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PAC with “Aberrant Conduction” Tachycardias

(Physiologic Delay in the His Purkinje System)

V1

P

P

P’

P

RBBB


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PACs with Aberrant Conduction Tachycardias

(Physiologic RBBB and LBBB)

V1

Normal

conduction

LBBB

RBBB


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PACs with Physiologic LBBB Tachycardias

and His-Purkinje System Block

V1

Non-conducted

PAC


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Non-Conducted PAC Tachycardias

V5

V1

P

P

P’

P

Note deformation of T wave by the PAC


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Bigeminal/Blocked PACs Tachycardias

Mimicking Sinus Bradycardia

V1

Only the 4th

bigeminal PAC

conducts


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Clinical Significance PAC’s Tachycardias

  • Common in the general population

  • May be associated with heart disease

  • Can be a precursor to atrial tachyarrhythmias


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Atrial Tachycardia Tachycardias

V1

  • RP intervals can be variable

  • RP often > 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 Tachycardias

  • Similar to sequela of AV junctional reentrant tachycardias

  • Must be differentiated from them diagnostically


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Atrial Flutter Tachycardias

(“Typical,” Counterclockwise)

Reentrant

mechanism


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Atrial Flutter Tachycardias

Classic

inverted

“sawtooth”

flutter waves

at 300 min-1

(best seen in

II, III and AVF)

II

2:1

4:1

V1

Note variable

ventricular

response


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Atrial Flutter Tachycardias

V. rate

140-160

beats/min

2:1

Conduction

(common)

2:1 & 3:2

Conduction

1:1

Conduction

(rare but

dangerous)


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Atrial Fibrillation Tachycardias

Focal firing

or

multiple

wavelets

Chaotic, rapid

atrial rate at

400-600

beats per min


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Atrial Fibrillation Tachycardias

V5

V1

  • Rapid, undulating baseline(best seen in V1)

  • Most impulses block in AV node Erratic conduction


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Atrial Fibrillation: Characteristic Tachycardias

“Irregularly Irregular” Ventricular Response

II


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Atrial Fibrillation with Tachycardias

Rapid Ventricular Response

II

Irregularity may be subtle


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Atrial Fibrillation: Autonomic Modulation Tachycardias

of Ventricular Response

Baseline

Immediately after exercise


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Clinical Significance of Atrial Flutter and Fibrillation Tachycardias

  • 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 Tachycardias

Ventricular Preexcitation


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Atrial Fibrillation with Tachycardias

Rapid Conduction Via Accessory Pathway


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Atrial Fibrillation with Tachycardias

Third Degree AV Block

V1

V5

Regular ventricular rate reflects dissociated

slow junctional escape rhythm


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Regular Tachycardias Narrow QRS Tachycardias


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Differential Diagnosis of TachycardiasRegular 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 (#P’s > #QRS’s), SVT is atrial in origin


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SVT Responses to AV Nodal Depressant Maneuvers Depressing AV Nodal Conduction

  • 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 Depressing AV Nodal Conduction

Stimulation of

carotid sinus

triggers

baroreceptor

reflex and

increased vagal

tone, affecting

SA and AV

nodes


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Termination of SVT by Depressing AV Nodal Conduction

Vagotonic Maneuver (Carotid Sinus Massage)


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SVT Depressing AV Nodal Conduction

Carotid Sinus Massage


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SVT Depressing AV Nodal Conduction

Adenosine 6 mg

P

P

P

P


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Ventricular Tachyarrhythmias Depressing AV Nodal Conduction


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Premature Ventricular Complex (PVC): Depressing AV Nodal Conduction Alternative Terminology

  • Premature ventricular contraction

  • Ventricular extrasystole

  • Ventricular premature beat

  • Ventricular ectopic beat

  • Ventricular premature depolarization


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Premature Ventricular Complex (PVC) Depressing AV Nodal Conduction

Compensatory

Pause


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PVCs: Bigeminal Pattern Depressing AV Nodal Conduction

“RegularlyIrregular” Rhythm


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Accelerated Idioventricular Rhythm Depressing AV Nodal Conduction

( Ventricular Escape Rate, but  100 bpm)

Fusion

beat

Sinus

acceleration

Ectopic

ventricular activation

Normal

ventricular activation


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AV Dissociation Depressing AV Nodal Conduction

ATRIA AND VENTRICLES

ACT INDEPENDENTLY

SA

Node

Ventricular

Focus


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Ventricular Tachycardia (VT) Depressing AV Nodal Conduction

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 Depressing AV Nodal Conduction

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 Depressing AV Nodal Conduction

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 Depressing AV Nodal Conduction


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Polymorphic VT Depressing AV Nodal Conduction

V1


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Causes of PVC’s and VT Depressing AV Nodal Conduction

  • PVC’s 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 PVC’s and VT


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MI Scar-Related Sustained Monomorphic VT Circuit Depressing AV Nodal Conduction


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“Torsade de Pointes” Depressing AV Nodal Conduction

(Polymorphic VT Associated with Prolonged Repolarization)


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Clinical Significance of PVC’s and VT Depressing AV Nodal Conduction

  • 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 Depressing AV Nodal Conduction

  • VT  250 beats/min, without clear isoelectric line

  • Note “sine wave”-like appearance


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Ventricular Fibrillation (VF) Depressing AV Nodal Conduction

  • Totally chaotic rapid ventricular rhythm

  • Often precipitated by VT

  • Fatal unless promptly terminated (DC shock)


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Sustained VT: Degeneration to VF Depressing AV Nodal Conduction


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Atrial Fibrillation with Rapid Conduction Depressing AV Nodal Conduction

Via Accessory Pathway: Degeneration to VF


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Diagnosing Depressing AV Nodal Conduction Regular

Wide QRS Tachycardia


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Regular Wide QRS Tachycardia: Depressing AV Nodal Conduction

VT or SVT with Aberrant Conduction?

V1


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Sustained Aberrant Conduction Depressing AV Nodal Conduction

V1


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Clinical Clues to Basis Depressing AV Nodal Conduction for Regular Wide QRS Tachycardia

  • REMEMBER: VT does not invariably cause hemodynamic collapse; patients may be conscious and stable

  • History of heart disease, especially priormyocardial 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: Depressing AV Nodal Conduction

VT or SVT with Aberrant Conduction?


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More Depressing AV Nodal Conduction R-Waves Than P-Waves Implies VT!

II


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Artifact Mimicking “Ventricular Tachycardia” Depressing AV Nodal Conduction

QRS complexes “march through”

the pseudo-tachyarrhythmia

Artifact

precedes

“VT”


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