Transcript Tachyarrhythmias

Cardiac Arrhythmias II: Tachyarrhythmias
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
Conduction
Unidirectional
Block
Recovery of
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
AP
Retrograde
conduction
via accessory
pathway (AP)
Anterogade
conduction
via normal
pathway
Initiation of Orthodromic
AV ReentrantTachycardia
PAC
Atria
AP
AVN
Ventricles
PAC = premature atrial
complex (beat)
Sustainment of Orthodromic
AV Reciprocating Tachycardia
Atria
AP
Rate 150-250
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
beat
Hybrid
QRS shape
“Delta” Wave
AP
Fusion activation
of the ventricles
PR < .12 s
QRS ≥ .12 s
Varying Degrees of
Ventricular Preexcitation
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
SVT:
V Preex
gone
Note
retrograde
P waves
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
P
P
P
Physiologic
AV Block
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
AV nodal or
AV reentrant
SVT
• RP intervals can be variable
• RP often > PR
• (Example slower than more common rate
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
II
4:1
V1
2:1
Classic
inverted
“sawtooth”
flutter waves
at 300 min-1
(best seen in
II, III and AVF)
Note variable
ventricular
response
Atrial Flutter
2:1
Conduction
(common)
2:1 & 3:2
Conduction
1:1
Conduction
(rare but
dangerous)
V. rate
140-160
beats/min
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;
sometimes see “lone “ atrial fibrillation
– Hyperthyroidism (atrial fibrillation)
but
• 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 “adenosinesensitive”)
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
PVCs: Bigeminal Pattern
“Regularly Irregular” Rhythm
Accelerated Idioventricular Rhythm
(> Ventricular Escape Rate, but < 100 bpm)
Fusion
beat
Ectopic
ventricular activation
Sinus
acceleration
Normal
ventricular activation
AV Dissociation
SA
Node
ATRIA AND
VENTRICLES
ACT INDEPENDENTLY
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”