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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
Cardiac Arrhythmias II: Tachyarrhythmias

Michael H. Lehmann, M.D.

Clinical Professor of Internal Medicine

Director, Electrocardiography Laboratory

supraventricular tachycardias
Supraventricular Tachycardias

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

slide3

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
slide4

AV Junctional Reentrant Tachycardias

(typically incorporate AV nodal tissue)

slide5

Mechanism of Reentry

Bidirectional

Conduction

Unidirectional

Block

Recovery of

Excitability

& Reentry

slide7

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

slide8

Initiation of AV Nodal Reentrant Tachycardia

PAC

PAC

PAC = premature atrial

complex (beat)

slide9

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

slide10

Sustained AV Nodal Reentrant Tachycardia

V1

P

P

P

P

Note fixed, short RP interval mimicking r’ deflection of QRS

slide11

Orthodromic AV Reentrant Tachycardia

Anterogade

conduction

via normal

pathway

AP

Retrograde

conduction

via accessory

pathway (AP)

slide12

Initiation of Orthodromic

AV ReentrantTachycardia

PAC

Atria

AP

AVN

Ventricles

PAC = premature atrial

complex (beat)

slide13

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

slide14

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

slide15

Varying Degrees of

Ventricular Preexcitation

slide17

Intermittent Accessory Pathway Conduction

V Preex

V Preex

Normal

Conduction

Note “all-or-none” nature of AP conduction

slide18

Orthodromic AV Reentrant Tachycardia

NSR with

V Preex

Note

retrograde

P waves

in the

ST segment

SVT:

V Preex

gone

slide19

Concealed Accessory Pathway

Sinus

beat

No Delta wave

during NSR

(but AP capable

of retrograde

conduction)

summary of av junctional reentrant tachycardias
Summary of AV Junctional Reentrant Tachycardias
  • Reentrant circuit incorporates AV nodal tissue
  • P waves generated retrogradely over a fast pathway
  • Short, fixed RP interval
clinical significance of av junctional reentrant tachycardias
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
slide23

Sinus Tachycardia (100 to 180+ beats/min)

  • P waves oriented normally
  • PR usually shorter than at rest
causes of sinus tachycardia
Causes of Sinus Tachycardia
  • Hypovolemia ( blood loss, dehydration)
  • Fever
  • Respiratory distress
  • Heart failure
  • Hyperthyroidism
  • Certain drugs (e.g., bronchodilators)
  • Physiologic states (exercise, excitement, etc)
slide25

Premature Atrial Complex (PAC)

V5

Non-Compensatory

Pause

P

P

P

P’

P

Timing of

Expected P

premature atrial complex pac alternative terminology
Premature Atrial Complex (PAC): Alternative Terminology
  • Premature atrial contraction
  • Atrial extrasystole
  • Atrial premature beat
  • Atrial ectopic beat
  • Atrial prematuredepolarization
slide27

PACs: Bigeminal Pattern

P

P’

P

P’

P

P’

  • Note deformation of T wave by the PAC
  • “RegularlyIrregular” Rhythm
slide28

PACs with Conduction Delay/Block

Physiologic

AV Block

P

P’

Physiologic

AV Delay

P

P’

Recovered

AV Conduction

P

P’

slide29

PAC with “Aberrant Conduction”

(Physiologic Delay in the His Purkinje System)

V1

P

P

P’

P

RBBB

slide30

PACs with Aberrant Conduction

(Physiologic RBBB and LBBB)

V1

Normal

conduction

LBBB

RBBB

slide31

PACs with Physiologic LBBB

and His-Purkinje System Block

V1

Non-conducted

PAC

slide32

Non-Conducted PAC

V5

V1

P

P

P’

P

Note deformation of T wave by the PAC

slide33

Bigeminal/Blocked PACs

Mimicking Sinus Bradycardia

V1

Only the 4th

bigeminal PAC

conducts

clinical significance pac s
Clinical Significance PAC’s
  • Common in the general population
  • May be associated with heart disease
  • Can be a precursor to atrial tachyarrhythmias
slide35

Atrial Tachycardia

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

clinical significance of atrial tachycardia
Clinical Significance of Atrial Tachycardia
  • Similar to sequela of AV junctional reentrant tachycardias
  • Must be differentiated from them diagnostically
slide37

Atrial Flutter

(“Typical,” Counterclockwise)

Reentrant

mechanism

slide38

Atrial Flutter

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

slide39

Atrial Flutter

V. rate

140-160

beats/min

2:1

Conduction

(common)

2:1 & 3:2

Conduction

1:1

Conduction

(rare but

dangerous)

slide40

Atrial Fibrillation

Focal firing

or

multiple

wavelets

Chaotic, rapid

atrial rate at

400-600

beats per min

slide41

Atrial Fibrillation

V5

V1

  • Rapid, undulating baseline(best seen in V1)
  • Most impulses block in AV node Erratic conduction
slide42

Atrial Fibrillation: Characteristic

“Irregularly Irregular” Ventricular Response

II

slide43

Atrial Fibrillation with

Rapid Ventricular Response

II

Irregularity may be subtle

slide44

Atrial Fibrillation: Autonomic Modulation

of Ventricular Response

Baseline

Immediately after exercise

clinical significance of atrial flutter and fibrillation
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
slide46

Varying Degrees of

Ventricular Preexcitation

slide47

Atrial Fibrillation with

Rapid Conduction Via Accessory Pathway

slide48

Atrial Fibrillation with

Third Degree AV Block

V1

V5

Regular ventricular rate reflects dissociated

slow junctional escape rhythm

differential diagnosis of regular narrow qrs supraventricular tachycardia
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
determining av nodal participation in svt by transiently depressing av nodal conduction
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
svt responses to av nodal depressant maneuvers
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”)
slide53

Carotid Sinus Massage

Stimulation of

carotid sinus

triggers

baroreceptor

reflex and

increased vagal

tone, affecting

SA and AV

nodes

slide54

Termination of SVT by

Vagotonic Maneuver (Carotid Sinus Massage)

slide55

SVT

Carotid Sinus Massage

slide56

SVT

Adenosine 6 mg

P

P

P

P

premature ventricular complex pvc alternative terminology
Premature Ventricular Complex (PVC): Alternative Terminology
  • Premature ventricular contraction
  • Ventricular extrasystole
  • Ventricular premature beat
  • Ventricular ectopic beat
  • Ventricular premature depolarization
slide61

PVCs: Bigeminal Pattern

“RegularlyIrregular” Rhythm

slide62

Accelerated Idioventricular Rhythm

( Ventricular Escape Rate, but  100 bpm)

Fusion

beat

Sinus

acceleration

Ectopic

ventricular activation

Normal

ventricular activation

slide63

AV Dissociation

ATRIA AND VENTRICLES

ACT INDEPENDENTLY

SA

Node

Ventricular

Focus

slide64

Ventricular Tachycardia (VT)

V1

  • Rates range from 100-250 beats/min
  • Non-sustained or sustained
  • P waves often dissociated (as seen here)
slide65

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

slide66

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

causes of pvc s and vt
Causes of PVC’s and VT
  • 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
slide71

“Torsade de Pointes”

(Polymorphic VT Associated with Prolonged Repolarization)

clinical significance of pvc s and vt
Clinical Significance of PVC’s 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
slide73

Ventricular Flutter

  • VT  250 beats/min, without clear isoelectric line
  • Note “sine wave”-like appearance
slide74

Ventricular Fibrillation (VF)

  • Totally chaotic rapid ventricular rhythm
  • Often precipitated by VT
  • Fatal unless promptly terminated (DC shock)
slide76

Atrial Fibrillation with Rapid Conduction

Via Accessory Pathway: Degeneration to VF

slide77

Diagnosing Regular

Wide QRS Tachycardia

slide78

Regular Wide QRS Tachycardia:

VT or SVT with Aberrant Conduction?

V1

clinical clues to basis for regular wide qrs tachycardia
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 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
slide81

Regular Wide QRS Tachycardia:

VT or SVT with Aberrant Conduction?

slide83

Artifact Mimicking “Ventricular Tachycardia”

QRS complexes “march through”

the pseudo-tachyarrhythmia

Artifact

precedes

“VT”

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