Transcript Class I: Na Channel Blockers

Tachydysrrhythmias
Lisa Campfens MD, FRCPC, FACEP
Generation of Dysrrhythmias
Two fundamental causes
Disturbances of automaticity
 Disturbances of conduction
 AV block
 Reentry
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Presentation
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Multiple symptoms:
Fatigue
Dyspnea
Presyncope
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Chest pain
Dizziness
Palpitations
Patients can be symptomatic even with single
premature beats or non-sustained atrial
arrhythmias
Complications
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SVTs common but persistent
Rarely life-threatening but present sig problems
in patient management
A fib/A flutter: Stroke 2°to embolization
Persistence of tachycardia :
Dilated cardiomyopathy
 CHF
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Referral
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All patients with wide complex tachycardia of
unknown origin
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Resistant/intolerant to pharmacological therapy
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WPW Syndrome
Classification of
Antidysrrhythmic Drugs
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Vaughan Williams classification
 Class I: Na channel blockers
 Class II: B blockers
 Class III: K channel blockers
 Class IV: Ca channel blockers
 Other: adenosine, digoxin, and ibutilide
Class I: Na Channel Blockers
Class IA
 Class IB
 Class IC

Quinidine, Procainamide
Lidocaine, Phenytoin, Mexilitine
Flecainide, Propafenone
Procainamide
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Therapeutic use
Ventricular tachycardia
 SVT with aberrancy
 Pre-excitation Syndromes
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Class II: Beta Blockers
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Metoprolol, Atenolol, Esmolol
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Therapeutic use
 Slow
ventricular rate (A fib/ A flutter)
 Terminate SVT caused by an AV nodal
reentrant circuit
Class II: Beta Blockers (cont’d)

Adverse effects
Heart block
 Heart failure
 AV block
 Sinus arrest
 Hypotension
 Bronchospasm (asthma/COPD)
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Class III: K Channel Blockers
Amiodarone
Therapeutic use

Life-threatening ventricular dysrrhythmias
SVT with aberrancy
 Pre-excitation Syndromes
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Class IV: Ca Channel Blockers
Verapamil, Diltiazem

Therapeutic use
Slow ventricular rate (A fib/ A flutter)
 Terminate SVT caused by an AV nodal reentrant
circuit

.
Other Antidysrhythmic Drugs
Adenosine
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Half-life few seconds
Intense but transient AV block thereby terminating
tachycardia
Safe in patients with heart disease
Contraindications: asthma/COPD
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Therapeutic use
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termination of PSVT
PSVTs
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A Fibrillation
A Flutter
AVNRT
AVRT (ORT)
Reentry
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Most common
mechanism
Requires two separate
paths of conduction
Requires an area of
slow conduction
Requires
unidirectional block
Regular SVT in Adults
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90% reentrant
60% AVNRT
30% AVRT (ORT)
10% Atrial tachycardia
2 to 5% involve WPW syndrome
AV Nodal Reentrant
Tachycardia Slow pathway
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Re-entrant circuit is
small and is in or
closely related to the
AV node
Fast pathway
AV Nodal Reentrant Tachycardia
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3o % respond to vagal
maneuvers
Very responsive to AVN
blocking agents: B blockers,
CA channel blockers,
adenosine.
Recurrences are the norm on
medical therapy
Catheter ablation 95%
successful with 1% major
complication rate
Orthodromic Reciprocating
Tachycardia
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Anterograde over AV
node and retrograde
conduction of an
accessory pathway.
Frequently presents in
patients with WPW as
narrow complex
tachycardia
Conduction down
AVnode
Up
accessory
pathway
ORT
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Amenable to AV nodal
blocking agents in
absence of WPW
syndrome (anterograde
conduction of pathway)
Amenable to catheter
ablation with 95%
success and 1% rate
major complication
Conduction down
AVnode
Up
accessory
pathway
Atrial Tachycardia
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Atrial rate 150-250 bpm
Does not require AVN or infranodal
conduction
P wave morphology different
PR interval > 120 ms differentiating from
junctional tachycardia
Atrial Tachycardia
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Left atrial focus- P wave upright V1/negative
in aVL
Right atrial focus-P wave negative V1/upright
in aVL
Adenosine may help with diagnosis
70-80% will also terminate with Adenosine.
Atrial Tachycardia
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Most are due to abn
automaticity and have
right atrial focus
May be reentry in
patients with prev
atriotomy scar, such as
CABG or congenital
repair patients
Atrial Tachycardia Therapy
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Antiarrhythmics
Class 1 : procainamide, quinidine, flecainide
Patients without structural heart disease.
 Class III : sotalol, amiodarone, dofetilide
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AVN blocking agents for rate control
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Catheter ablation effective in 70-80%
Atrial Flutter
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Rate 250 to 350 bpm
Rotates counter-clockwise
around right atrium using a
protected isthmus
Negative saw-tooth pattern
leads II , III, AVF and
positive in lead V1
Treatment similar to atrial
tachycardia but rate control
more difficult
Atrial Flutter and Risk of Stroke
Although risk of stroke historically thought to
be low, multiple instances of stroke with
cardioversion lead to similar indication for
anticoagulation as AF
42 year old smoker presents to the ED with
palpitations. BP 100/60.
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A. Emergent cardioversion for polymorphicVT
B. IV procainamide
C. IV lidocaine
D. IV diltiazem to obtain rate control.
Answer
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WPW with AF and a rapid ventricular
response. He is stable, thus IV procainamide
indicated to slow conduction down the
accessory pathway
Diltiazem contraindicated
Lidocaine will have no effect, as is not VT
Epidemiology of AF
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Affects 2-4% of population
Increases to 5-10 % >80 yrs
2-fold increased risk of death
15-25% of all strokes in US attributed to AF
Risk of thromboembolism approx 5%/yr but
may be as high as 20% in high risk groups not
anticoagulated
Management of Atrial
Fibrillation
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Symptom relief by rate and rhythm control
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Reduce risk of thromboembolism by
anticoagulation
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Prevent tachycardia-mediated cardiomyopathy
Acute Management of AF
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Focus on rate control
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DC cardioversion or pharmacologic conversion
if <48 hrs or following TEE on Heparin
without evidence of left atrial thrombus
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Following cardioversion anticoagulate for 4 wks
with goal INR of 2-3 until atrial fx normalizes**
Acute Management of AF
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50% spontaneously convert <24 hours
Digoxin used heavily in past for prevention/
conversion, ineffective at either
May be profibrillatory as decreases atrial
refractory period
Acute Management of Atrial
Fibrillation
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Rate control: Ca channel blockers or B blockers in
patients with normal LV fx
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Cautious use of Ca channel blockers if depressed
LV fx. Associated with increased mortality in long
term.
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Avoid Beta blockers in acutely decompensated CHF
patients with AF
AF and Depressed LV Fx
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Digoxin and amiodarone may be effective if LV
dysfx and decompensated CHF to slow
ventricular response.
Digoxin alone rarely effective when patient
sympathetically driven
Avoid high dose digoxin with amiodarone as
digoxin levels increase 2-fold with amiodarone
Chronic Management of AF
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Maintenance of sinus similar with class I and
class III drugs-50% recurrence at 1 year
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Recurrence of AF 80% at 1 year without
treatment
Chronic Management of AF
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Recent large trials reveal no benefit of rhythm vs rate
control
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Trend of increased mortality in rhythm arm
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Patients unable to tolerate AF due to symptoms were
not enrolled in these studies and are increasingly
undergoing ablation , catheter and surgical procedures.
Wide ComplexTachycardias
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Ventricular Tachycardia
SVT with aberrancy (functional bundle branch
block)
SVT with underlying bundle branch block
SVT with pre-excitation
Additional Mimimics of Wide
Complex Tachycardias
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SVT with severe hyperkalemia
SVT with use of antiarrhythmic agents
particularly 1C agents
SVT with acute MI
Wide-Complex Tachycardia
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Majority are SVT with BBB
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In higher risk population VT until proven
otherwise
Differentiating VT from SVT
with Aberrancy
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Leads to correct initial therapy
Verapamil may ppt hemodynamic collapse
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Hemodynamic status or rate not a clue to
mechanism
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In higher risk population VT until proven
otherwise
ECG criteria for diagnosis
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The Brugada Criteria
Table I.
Diagnosis Of Wide QRS Complex Tachycardia With A Regular Rhythm
Step 1. Is there absence of an RS complex in all precordial leads V1 – V6?
If yes, then the rhythm is VT.

Sens 0.21 Spec 1.0
Step 2. Is the interval from the onset of the R wave to the nadir of the S
wave greater than 100 msec in any precordial leads?
If yes, then the rhythm is VT.

Sens 0.66 Spec 0.98
Step 3. Is there AV dissociation?
If yes, then the rhythm is VT.

Sens 0.82 Spec 0.98
Step 4. Are morphology criteria for VT present? See Table II.
If yes, then the rhythm is VT.

Sens 0.99 Spec 0.97
Morphology Criteria for VT
Table II.
Morphology Criteria for VT
Right bundle type requires waveform from both V1 and V6.
V1
V6
Monophasic R wave
QR
or
QS
RS
or
QR
R/S <1
Left bundle type requires any of the below morphologies.
V1or V2
V6
R wave > 30 msec
QR
or
QS
Notched downstroke
S wave.
Greater than 60msec
nadir S wave.
Adapted from Brugada et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex.
Circulation 1991; 83:1649-59.
Therapy for VT
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Stable-chemical or DC cardioversion
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Unstable-DC cardioversion
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Amiodarone 150 mg IV over 10 mins, max 2.2
gm/24 hrs class IIA recommendation
New ACLS Algorithm
VT with Depressed LV Fx
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Amiodarone drug of choice
mortality neutral or beneficial
 Initial dose 150 mg IV. over 10 mins
 effective in VF using 300 mg bolus with improved
arrival to hospital.
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DC cardioversion always acceptable option
Procainamide contraindicated
VT with Preserved LV Fx
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DC cardioversion
Amiodarone 1st line RX according to ACLS
Procainamide
Lidocaine
Avoid use of combination antiarrhythmic agents
AVRT Extranodal Accessory
Pathways and WPW Syndrome
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Extremely symptomatic but rarely observed
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In the presence of AF, VF can occur if the
refractory period of the accessory pathway is
<250 msec
WPW
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Not an arrhythmia but a clinical syndrome
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ECG: PR<.12 sec, QRS>.10 sec, delta wave
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Many types of arrhythmias
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‘Is AVN an integral part or an innocent
bystander?’
WPW
AV Node Integral
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AVRT-Orthodromic
AV blocking diagnostic and therapeutic
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AVRT-Antidromic
Regular
AV blocking diagnostic and therapeutic
WPW
AV Node Innocent Bystander
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AF
Can be serious problem
Polymorphic VT
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Immediate defibrillation
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IV Lidocaine , Amiodarone
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Usually result of severe metabolic disturbance or
cardiac ischemia.
Monomorphic VT in Patients with
Normal LV Fx
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No structural heart disease
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Present as palpitations, syncope but rarely as
sudden death
Monomorphic VT in Patients with
Normal LV Fx
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RV outflow tachycardia
 LBB morphology inferior axis
 adenosine, Calcium channel , occ beta blockers
 Amenable to Ablation
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Idiopathic LV tachycardia
 RBB superior axis
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Verapamil and adenosine sensitive
 Amenable to Ablation
Torsades de Pointes
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Polymorphic VT assoc with long QT
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Frequently initiated after pause
Iatrogenic
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QTc >440msec , QT > 500 msec
hypoK, hypoMg, Hypo Ca, Drugs, Combination
Congenital
QT Prolonging or Torsadogenic Drugs
The following drugs have been shown to prolong the QT interval or have documented clinical Torsades de Pointes reported in the literature
Amantadine
Quetiapine
Aminophylline
Quinidine
Amiodarone
Risperdone
Barium
Salmeterol
Bepridil
Thioridazine
Chloralhydrate
Sparfloxacin
Chloroquine
Sumatriptan
Ciprofloxacin
Tacrilimus
Cisapride
Tamoxifen
Sertraline
Chlorpromazine
Disopyramide
Tizanide
Dofetilide
Trimethorprim
Sulfa
Doxepine
Venlafaxine
Droperidol
Vistaril
Sotalol
Flecanide
Fluoxetine
Foscarnet
Fosphentoin
Gatifloxin
Halofantrine
Haloperidol
Ibutilide
Imipramine
Indipamide
Isradapine
Ketaconazole
Levofloxacin
Levomethadyl
Mesoridazine
Moexitine/Hctz
Moxifloxicin
Naratripan
Nicardipine
Octreotide
Pentamidine
Pimozide
Probucol
Erythromycin
Zolmitriptan
Felbamate
Clarithromycin
Terfenadine
Desipramine
Treatment of Torsades de Pointes
Goal to shorten QT
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Remove offending agent
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Replete K
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IV Mg even if normal level
Treatment of Torsades de Pointes
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Overdrive pacing
isoproterenol
 Pacing
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DC Cardioversion
Rarely required
 May be refractory
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Sudden Death with Normal
LV Fx
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Brugada Syndrome
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Incompete RBB ST elevation V1V2
RV Dysplasia
Delayed RV activation
 Epsilon wave , deep precordial Twave inversion
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Sudden Death with Normal
LV FX
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Hypertrophic Cardiomyopathy
Major cause in U.S. in young patients without CAD
 Risk factors
 ICD effective
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67 yr old male with prior infarct and LV dysfx presents with
palpitations and dizziness. BP is 80/40
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A. Synchronized cardioversion for VT
B. IV Procainamide for AF with WPW
syndrome
C. Synchronized cardioversion for unstable
SVT with aberrancy.
D. IV Amiodarone for SVT with aberrancy in
a patient with LV dysfx
Answer

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This patient has VT. An RS interval >100 msec
clearly visible. In addition, by history this patient
is overwhelmingly likely to present with VT with
a wide complex rhythm
Unstable with relative hypotension requiring
immediate cardioversion as opposed to
pharmacologic therapy.
46 yr old alcoholic, on methadone, with
schizophrenia. She began feeling dizzy after starting
a fluoroquinalone for a UTI
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A. Administer IV Procainamide
B. Consult EP for placement of a ICD
C. Discontinue antibiotic and antipsychotic, treat
with IV Mg, and consider temporary pacing
D. Administer IV Amiodarone
Answer
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Torsades de Pointes with classic polymorphic
VT and prolonged QT demonstrated on bottom
strip.
Procainamide or amiodarone would worsen this
rhythm.
ICD is not indicated .