Cardiac Arrhythmias II:

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

(Supraventricular - a rhythm process in which

the ventricles are activated from the atria or
AV node/His bundle region)
 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
AV Junctional Reentrant Tachycardias
(typically incorporate AV nodal tissue)
 Mechanism of Reentry

Bidirectional Unidirectional Recovery of

Conduction Block Excitability
& Reentry
AV Nodal Reentrant Tachycardia
 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
 Initiation of AV Nodal Reentrant Tachycardia

PAC

PAC

PAC = premature atrial

complex (beat)
 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
Sustained AV Nodal Reentrant Tachycardia

V1

P P P P

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

 Orthodromic AV Reentrant Tachycardia

Anterogade
conduction
AP via normal
Retrograde pathway
conduction
via accessory
pathway (AP)
 Initiation of Orthodromic
AV ReentrantTachycardia
PAC

Atria

AP

AVN

Ventricles

PAC = premature atrial

complex (beat)
 Sustainment of Orthodromic
AV Reciprocating Tachycardia

Atria
Rate 150-250
AP beats per min

AVN

Ventricles
Retrograde P’s fall
in the ST segment
with fixed, short RP
 Accessory Pathway with
Ventricular Preexcitation
(Wolff-Parkinson-White Syndrome)
Sinus Hybrid
beat “Delta” Wave
QRS shape
PR < .12 s
AP

Fusion activation QRS  .12 s

of the ventricles
 Varying Degrees of
Ventricular Preexcitation
QRS Width: Synchronous vs. Asynchronous
Ventricular Activation
QRS
Normal synchronous
overlapping activation Narrow
of both ventricles:

On
time Late
Asynchronous Wide
scenario I:

On
Head start time
(or late) Wide
Asynchronous
scenario II:
Intermittent Accessory Pathway Conduction

V Preex V Preex
Normal
Conduction

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

 Orthodromic AV Reentrant Tachycardia

NSR with
V Preex

Note
SVT: retrograde
V Preex P waves
gone in the
ST segment
 Concealed Accessory Pathway

Sinus
beat

No Delta wave
during NSR
(but AP capable
of retrograde
conduction)
 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
• 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
Atrial Tachyarrhythmias
Sinus Tachycardia (100 to 180+ beats/min)

• P waves oriented normally

• PR usually shorter than at rest
 Causes of Sinus Tachycardia

• Hypovolemia ( blood loss, dehydration)

• Fever
• Respiratory distress
• Heart failure
• Hyperthyroidism
• Certain drugs (e.g., bronchodilators)
• Physiologic states (exercise, excitement, etc)
 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 contraction
• Atrial extrasystole
• Atrial premature beat
• Atrial ectopic beat
• Atrial premature depolarization
 PACs: Bigeminal Pattern

P P’ P P’ P P’

• Note deformation of T wave by the PAC

• “Regularly Irregular” Rhythm
PACs with Conduction Delay/Block

Physiologic
P P’
AV Block

P P’ Physiologic
AV Delay

P P’ Recovered
AV Conduction
 PAC with “Aberrant Conduction”
(Physiologic Delay in the His Purkinje System)

V1

P P P’ P

RBBB
 PACs with Aberrant Conduction
(Physiologic RBBB and LBBB)

V1

RBBB LBBB Normal

conduction
 PACs with Physiologic LBBB
and His-Purkinje System Block

V1
Non-conducted
PAC
 Non-Conducted PAC
V5

V1
P P P’ P

Note deformation of T wave by the PAC

 Bigeminal/Blocked PACs
Mimicking Sinus Bradycardia

V1

Only the 4th

bigeminal PAC
conducts
 Clinical Significance PAC’s

• Common in the general population

• May be associated with heart disease
• Can be a precursor to atrial tachyarrhythmias
 Atrial Tachycardia

V1

Differs from • RP intervals can be variable

AV nodal or • RP often > PR
AV reentrant • (Example slower than more common rate
SVT
mof 150-250 beats per min)
 Clinical Significance of Atrial
Tachycardia
• Similar to sequela of AV junctional reentrant
tachycardias

• Must be differentiated from them diagnostically

 Atrial Flutter
(“Typical,” Counterclockwise)

Reentrant
mechanism
 Atrial Flutter

Classic
II inverted
“sawtooth”
flutter waves
4:1 2:1 at 300 min-1
(best seen in
V1 II, III and AVF)

Note variable
ventricular
response
 Atrial Flutter

2:1 V. rate
Conduction 140-160
(common) beats/min

2:1 & 3:2

Conduction

1:1
Conduction
(rare but
dangerous)
 Atrial Fibrillation

Focal firing
or
multiple
wavelets Chaotic, rapid
atrial rate at
400-600
beats per min
 Atrial Fibrillation

V5

V1

• Rapid, undulating baseline (best seen in V1)

• Most impulses block in AV node  Erratic conduction
 Atrial Fibrillation: Characteristic
“Irregularly Irregular” Ventricular Response

II
 Atrial Fibrillation with
Rapid Ventricular Response

II

Irregularity may be subtle

 Atrial Fibrillation: Autonomic Modulation
of Ventricular Response
Baseline

Immediately after exercise

 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
 Varying Degrees of
Ventricular Preexcitation
 Atrial Fibrillation with
Rapid Conduction Via Accessory Pathway
 Atrial Fibrillation with
Third Degree AV Block

V1

V5

Regular ventricular rate reflects dissociated

slow junctional escape rhythm
Regular Narrow QRS Tachycardias
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
• 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 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”)
Carotid Sinus Massage

Stimulation of
carotid sinus
triggers
baroreceptor
reflex and
increased vagal
tone, affecting
SA and AV
nodes
 Termination of SVT by
Vagotonic Maneuver (Carotid Sinus Massage)
SVT

Carotid Sinus Massage

SVT

Adenosine 6 mg

P P P P
Ventricular Tachyarrhythmias
 Premature Ventricular Complex (PVC):
Alternative Terminology
• Premature ventricular contraction
• Ventricular extrasystole
• Ventricular premature beat
• Ventricular ectopic beat
• Ventricular premature depolarization
Premature Ventricular Complex (PVC)

Compensatory
Pause
QRS Width: Synchronous vs. Asynchronous
Ventricular Activation
QRS
Normal synchronous
overlapping activation Narrow
of both ventricles:

On
time Late
Asynchronous Wide
scenario I:

On
Head start time
(or late) Wide
Asynchronous
scenario II:
PVCs: Bigeminal Pattern

“Regularly Irregular” Rhythm

 Accelerated Idioventricular Rhythm
( Ventricular Escape Rate, but  100 bpm)

Fusion
beat
Ectopic Sinus Normal
ventricular activation acceleration ventricular activation
 AV Dissociation

ATRIA AND
VENTRICLES
SA ACT INDEPENDENTLY
Node

Ventricular
Focus
 Ventricular Tachycardia (VT)

V1

• Rates range from 100-250 beats/min

• Non-sustained or sustained
• P waves often dissociated (as seen here)
 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
 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
Monomorphic VT
 Polymorphic VT

V1
 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
MI Scar-Related Sustained
Monomorphic VT Circuit
 “Torsade de Pointes”
(Polymorphic VT Associated with Prolonged
Repolarization)
 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
 Ventricular Flutter

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

• Note “sine wave”-like appearance
Ventricular Fibrillation (VF)

• Totally chaotic rapid ventricular rhythm

• Often precipitated by VT
• Fatal unless promptly terminated (DC shock)
Sustained VT: Degeneration to VF
Atrial Fibrillation with Rapid Conduction
Via Accessory Pathway: Degeneration to VF
Diagnosing Regular
Wide QRS Tachycardia
 Regular Wide QRS Tachycardia:
VT or SVT with Aberrant Conduction?

V1
 Sustained Aberrant Conduction

V1
 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
 Regular Wide QRS Tachycardia:
VT or SVT with Aberrant Conduction?
More R-Waves Than P-Waves Implies VT!

II
Artifact Mimicking “Ventricular Tachycardia”

QRS complexes “march through”

the pseudo-tachyarrhythmia

Artifact
precedes
“VT”