Download Approach to Arrhythmias

Approach to Arrhythmias
Armed Forces Academy of
Medical Sciences
When to Suspect an Arrhythmia
Symptoms variable and depend on rate of
ventricular response, overall condition of patient,
presence of structural heart disease
 Palpitations (regular vs. irregular, onset/offset)
 Chest pressure
 Dyspnea
 Lightheadedness, presyncope, syncope
Triggers
Termination maneuvers: especially vagal
First Question
Stable vs. Unstable


Unstable: hypotensive, syncope, imminent
death
Unstable: revert to ACLS algorithm
DC Cardioversion

Most likely ventricular arrhythmia
Stable

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Symptoms but not life threatening
Differentiate wide complex from narrow
complex
Initial Evaluation of Stable
Arrhythmias
History
Physical exam
EKG (sinus rhythm, tachycardia)

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Twelve lead ECG with and without symptoms
Narrow complex: likely a superventricular
tachycardia (SVT)
Wide complex
Ventricular arrhythmia
SVT with aberrant conduction
Echo if structural heart disease suspected
SVTs
Any tachycardia requiring the atrium or the AVN
for its perpetuation
Common arrhythmia with an incidence of
2.5/1000

Twice as common in women
Three primary etiologies

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AVNRT (most common)
AVRT
Atrial tachycardia (least common in absence of
structural heart disease)
Rare: IST, SNRT, junctional tachycardia
SVTs Continued
Can present at any age, first symptoms occur
from 12 to 30 years

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AVNRT: middle to older age
AVRT: adolescence
Usually occurs in absence of structural heart
disease

Exceptions: Ebstein’s anomaly, familial preexcitation
with hypertrophy, atrial tachycardia
Classification of SVTs
AV node dependent vs. independent

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AT: independent
AVNRT, AVRT: dependent
Short RP vs. Long RP

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Short RP (RP<PR): typical AVNRT, AVRT
Long RP (PR<RP): AT, atypical AVNRT, rare forms of
AVRT
Regular vs. irregular

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Regular: AVNRT, AVRT, AT, AFL
Irregular: AF, AT, AFL
Paroxysmal Supraventricular Tachycardias: Short
RP vs. Long RP
no p-wave
- AV node reentry
AVNRT
AT
RP < PR
- AV node reentry
- AV reentry using an
accessory pathway
AVRT
RP > PR
- Atrial tachycardia
- AV reentry using a
decremental AP
ex. PJRT
- AV node reentry atypical/uncommon form
Differential Diagnosis of NCT
AVNRT
Most common form of Paroxysmal SVT

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50-60% of regular, narrow complex tachycardias
Usual rate: 150-250 bpm
Prototypic patient: young to middle age, healthy
female with no Structural Heart Disease
Palpitations with sudden onset/offset, may be
terminated by maneuvers that lead to AVN block


Vagal maneuvers
Adenosine
AVNRT
Mechanism: Reentry
Required substrate: dual AV nodal physiology

At least 2 separate pathways provide input into the
AVN
Fast pathway: rapid conduction, slower recovery
Slow pathway: slow conduction, rapid recovery
Typical form: short RP


P waves not seen due to simultaneous A and V
activation
P waves distort terminal QRS pseudo r’ in v1,
pseudo S waves in inferior leads
Reentry in AVNRT
A: slow B: fast
3 prerequisites
 2 anatomically or
functionally distinct
conduction
pathways
 Unidirectional block
in 1 pathway
 Slowed conduction
down second
pathway
Sinus Rhythm
PAC
Reentry
42 yo female with sudden onset palpitations, no PMHx
Typical AVNRT
AVNRT Acute Management
Hemodynamically unstable

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Very rare with AVNRT
Use ACLS algorithm
Vagal Maneuvers
Adenosine
Hemodynamically stable
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99% of all AVNRT cases
Vagal maneuvers, adenosine, verapamil,
diltiazem (Class 1)
BB, digoxin, amiodarone (Class 2b)
* Digoxin may be ineffective because its pharmacologic effects can be overridden by enhanced sympathetic tone
AVNRT Chronic Management
Determined by tolerance and frequency
Well tolerated, spontaneous or easy termination

Lifestyle modification, vagal maneuvers
More frequent or bothersome attacks

Pharmacotherapy-prophylactic, overall efficacy 30-65%
Slow AVN conduction
 BB, verapamil, diltiazem, digoxin*
Antiarrhythmic agents: Class Ic (no SHD) , III
 Daily therapy
 Pill-in-the-pocket (infrequent, prolonged,
well-tolerated): flecainide, diltiazem + propranolol
Frequent attacks despite prophylactic therapy

Catheter ablation: slow pathway
90-95% success, 1% risk of permanent AV block
AVRT
Accounts for 30% of regular, NCTs
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More common in males
Presents at younger age than AVNRT
Extranodal accessory pathway connects
myocardium of atrium to ventricle
May exhibit antegrade (orthodromic) and
retrograde conduction (antidromic)
Antegrade conduction results in delta wave on
surface EKG
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Incidence is 0.1 to 0.3% in general population
Classified based on location along the TV or MV annulus
Degree of preexcitation determined by relative
conduction to ventricle over the AVN vs. AP
Minimal preexcitation: latent
Preexcitation Pattern
Types of AVRT
Antegrade / Orthodromic
Retrograde / Antidromic
AVNRT
Conduction down accessory pathway is
usually rapid, nondecremental
During tachycardia if action potential
conducted down accessory pathway can
have 1:1 conduction

Atrial fibrillation or flutter could lead to
ventricular tachycardia
18 year old male with palpitations
18 year old male with palpitations
AV Reentry - retrograde
accessory pathway
conduction
p
p
Sinus rhythm - antegrade
accessory pathway
conduction
delta -wave
AVRT Acute Management
Orthodromic (NCT)-same as AVNRT
Antidromic (WCT)-goal: slow AP conduction
Unless there is strong evidence supporting AVN
dependence, adenosine, non-DHP CCB should be
avoided
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Ventricular rate may increase in WCT due to AT or
AFL with AP bystander conduction
AVN blocking agents ineffective in AP-AP
tachycardias
Adenosine may produce AF with rapid ventricular
rate
Procainamide, ibutilide IV are agents of choice
Pre-excited atrial fibrillation: slow AP conduction,
convert AF
Procainamide, ibutilide IV, DCCV if unstable
AVRT-Antidromic
25 yo with a long history of tachypalpitations
Preexcited Atrial Fibrillation
Unstable: DCCV
IV: procainamide, ibutilide
Avoid agents that slow AV nodal
conduction
EPS/RFA
AVRT Chronic Management
Management guided by presence of pre-excitation,
arrhythmia tolerance
 Concealed AP: pharmacologic management same as
for AVNRT
Pharmacologic therapy
 AVN blocking agents
Verapamil, diltiazem, digoxin contraindicated with
manifest pre-excitation
 Slow AP conduction-Class 1c,III antiarrhythmics
Catheter ablation: Class 1 for manifest preexcitation with
symptoms, poorly tolerated AVRT with concealed AP
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95% success, 5% recurrence (higher for right-sided and septal
APs)
Risk location dependent: AV block, perforation,
embolism

Overall major complication rate should be <3%
Focal Atrial Tachycardia
Uncommon SVT in structurally normal hearts, common with SHD (atrial
scarring)
Clinical forms

Incessant: tachycardia-induced cardiomyopathy
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Paroxysmal
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Nonsustained (very common on holters)
Mechanisms: triggered activity, enhanced automaticity, reentry (micro)
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Rapid spread of activation from focal site
Atrial rates 100 to 250bpm (rarely up to 300 bpm)
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Isoelectric baseline usually present between p waves
Distinguishes focal AT from AFL
AV blocks occurs
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AVN and ventricle are not required
PR/RP interval depend on AV nodal conduction properties
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Long RP tachycardia-most common
P wave morphology depends on site of origin in atrium
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P wave often obscured by T wave
62 year old female with occasional palpitations
P Waves in Atrial Tachycardia
V1
AVL
SVC
Left atrium
Lateral Left Atrium
Right Atrium
IVC
Septal: narrow p wave
Cranial: (+) in inferior leads
Caudal: (-) in inferior leads
Tang et al JACC 1995
Focal Atrial Tachycardia: Sites of Origin
RA: 75-85%
SVC
-Crista
terminalis
-TVA
Other: 5-10%
X
RA App
-CS os (7%)
LA
-SVC
-RAA
X
LA: 10-15%
-PVs (deep)
-IVC
-MVA
-Vein of
Marshall
-PV ostia
-CS muscle
RA
-LAA
*can be generators
for AF
IVC
Atrial Tachycardia Acute Treatment
Hemodynamically unstable (rare): DCCV

Terminates microreentry, triggered activity
Hemodynamically stable

Response/efficacy depends on mechanism
Adenosine (2a)
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Termination: triggered activity
Persistence with AV block: microreentry
Transient atrial slowing: automaticity
IV beta-blockers, CCB
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Termination (2a)
Rate control through AV block (1)
Second line: Ia, Ic, III AAD (2a) for direct
suppression
Focal Atrial Tachycardia: Chronic Management
AT
Pharmacologic
Beta-blockers
CCBs
Class Ia, Ic, or III antiarrhythmic drugs
Catheter Ablation: Efficacy: 80%-85% acute
Drug refractory or incessant
-tachycardia-induced CMP
Problems:
Inability to induce tachycardia
Multiple tachycardias (10%)
Nonsustained tachycardia
Recurrence (8-10%)
Focal Atrial Tachycardia
Middle-aged women with palpitations
Multifocal Atrial Tachycardia
Differential Diagnosis of
Wide-Complex Tachycardia
VT
SVT with aberrancy (atrial fibrillation/flutter)
Antidromic AV reentry via WPW accessory
pathway
Atrial fibrillation, atrial flutter, atrial
tachycardia, or AV nodal reentry in setting
of WPW with rapid conduction down
accessory pathway
Bundle branch reentry
Key ECG Signs
Atrial activity
Width of QRS
QRS Axis
QRS Configuration
Identifying Atrial Activity
P wave morphology
relationship between P and QRS

Capture beats
AV Dissociation a Hallmark, yet VA
conduction may be present
Physical Exam- JVP, S1, SBP,
Response to carotid sinus message
QRS Width
QRS width
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Wellens. Heart 2001;86:579-585
Site of origin- lateral
wall vs. near septum
Scar tissue, LVH,
HCM
>140ms in RBBB,
>160ms LBBB; likely
VT
Septal origin may
be narrower
VT likely if width
narrower than with
sinus rhythm
QRS Axis
Assists in
differentiation,
localization and
assessing etiology
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Inferior Axis- Basal
origin
Superior Axis- Apical
origin
Wellens et al. (Am J
Med 1978)- RBBB with
superior axis strongly
suggests VT
LBBB with inferior axis
argues for RVOT
tachycardia
Wellens. Heart 2001;86:579-585
QRS Configuration
Capture and Fusion Beats
Leads V1 and V6
QRS intervals
Concordance
QR complexes
Capture and Fusion Beats
Capture
Fusion
Wellens. Heart 2001;86:579-585
A-V Dissociation, Fusion, and
Capture Beats in VT
V1
E
ECTOPY
F
C
FUSION
Fisch C. Electrocardiography of Arrhythmias. 1990;134.
CAPTURE
Concordanc
e
Precodial
leads share
the same
axis

positive or
negative
Wellens. Heart 2001;86:579-585
Summary ECG Distinctions of VT from
SVT with Aberrancy
Favors VT
Duration
RBBB:
LBBB:
QRS > 0.14 sec.
QRS > 0.16 sec.
Axis
QRS axis -90° to ±180°
Favors SVT
with Aberrancy
< 0.14 sec.
< 0.16 sec.
Normal
Summary ECG Distinctions of VT from
SVT with Aberrancy
Favors VT
Favors SVT
with Aberrancy
Morphology
Precordial concordance
If LBBB:
R V1 duration > 30 ms
S wave > 70 ms
S wave notched or slurred
V6: qR or QR
R wave
monophasic
If RBBB:
V1: monophasic R wave
qR
If triphasic, R > R1
V6: R < S
R < R1
Additional Features
Left axis deviation >-30 useful
Right axis deviation >+90 w/ LBBB pattern
R to S nadir >100ms in 1 or more
precordial leads
QR complexes