Transcript Tachyarrhythmias, Diagnosis and Management

Tachyarrhythmias,
Diagnosis and Management
Laurent Lewkowiez, MD
Assistant Professor
Denver Health and Hospitals
University of Colorado Health
Sciences
Mechanisms of Arrhythmia
• Abnormal automaticity
– automatic impulse generation from unusual site
or overtakes sinus node
• Triggered activity
– secondary depolarization during or after
repolarization
– Dig toxicity, Torsades de Pointes
• Reentry
– 90 % of arrhythmias
Reentry
• Most common
mechanism
• Requires two separate
paths of conduction
• Requires an area of
slow conduction
• Requires
unidirectional block
Supraventricular Tachycardias
Diagnosis
• ECG is cornerstone
• Observe zones of transition for clues as to
mechanism:
–
–
–
–
onset
termination
slowing, AV nodal block
bundle branch block
Regular SVT in adults
• 90% reentrant 10 % not reentrant
• 60% AV nodal reentrant tachycardia (AVNRT)
• 30% orthodromic reciprocating tachycardia
(ORT)
• 10% Atrial tachycardia
• 2 to 5% involve WPW syndrome
Differential Dx of Regular SVT
• Short RP tachycardia
– AV nodal reentrant
tachycardia
– ORT( Orthodromic
reciprocating
tachycardia)
– atrial tachycardia when
associated with slow
AV nodal conduction
Short RP interval
AV Nodal Reentrant Tachycardia
Slow pathway
• 2 pathways within or limited to
perinodal tissue
– anterograde conduction
down fast pathway blocks
with conduction down slow
pathway, with retrograde
conduction up fast pathway.
• May have very short RP
interval with retrograde P wave
visible as an R’ in lead V1 or
psuedo-S wave in inferior leads
in 1/3 of cases . No p wave seen
in 2/3
Fast pathway
AV Nodal Reentrant Tachycardia
• Responds to vagal
maneuvers in 1/3 cases
• Very responsive to AV nodal
blocking agents such as beta
blockers, CA channel
blockers, adenosine.
• Recurrences are the norm on
medical therapy
• Catheter ablation 95%
successful with 1% major
complication rate
Ablation AVNRT
His bundle
Ablation
area
Orthodromic Reciprocating
Tachycardia
• Anterograde over AV node and
retrograde conduction of an
accessory pathway.
• RP interval short but longer
than AVNRT due to required
conduction through ventricle
prior to conduction up
accessory pathway
• Frequently presents in patients
with WPW patients as narrow
complex tachycardia
Conduction down
AVnode
Up
accessory
pathway
ORT
• 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
Differential Dx of Regular SVT
• Long RP tachycardia
–
–
–
–
Atrial tachycardia
Sinus node reentry
Sinus tachycardia
Atypical AV nodal
reentrant tachycardia
– Permanent form of
junctional reciprocating
tachycardia
Long RP interval
Atrial Tachycardia
• Atrial rate between 150 and 250 bpm
• Does not require AV nodal or infranodal
conduction
• P wave morphology different than sinus
• P-R interval > 120 msec differentiating from
junctional tachycardia
• Origin inferred from P wave morphology.
Atrial tachycardia
• P wave upright lead V1 and negative in aVL
consistent with left atrial focus.
• P wave negative in V1 and upright in aVL
consistent with right atrial focus.
• Adenosine may help with diagnosis if AV block
occurs and continued arrhythmia likely atrial
tachycardia
• 70-80% will also terminate with adenosine.
Atrial Tachycardia
• Most are due to
abnormal automaticity
and have right atrial
focus
• May be reentry
particularly in patients
with previous atriotomy
scar, such as CABG or
congenital repair patients
Atrial Tachycardia Therapy
• Frequently treated with antiarrhythmics
– Class 1 agents procainamide, quinidine, flecainide
may be used in patients without structural heart
disease.
– Class III agents sotalol, amiodarone, dofetilide
may be used with caution according to specific
side effects
• AV Nodal blocking agents for rate control.
• Catheter ablation effective in 70-80%
Other Long RP tachycardias
• Sinus node reentrant
– abrupt onset and offset
– P wave complex same as
sinus
– Amenable to calcium
channel blockers, much
less responsive to beta
blockers
– Amenable to catheter
ablation
• Syndrome of
inappropriate sinus
tachycardia
– typical sinus tachycardia
with lowest rate on Holter
of 130 bpm
– Treated with high dose
beta blockers
– Poor results with catheter
ablation
Atrial Flutter
• 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
Atrial Flutter and Risk of Stroke
• Although risk of stroke historically has been
thought to be low, multiple instances of
stroke with cardioversion lead to similar
indication for anticoagulation as atrial
fibrillation.
A 32 year old female is treated in the emergency room
for palpitations. The first ECG is tachycardia and the
second is after adensosine.What is the arrhythmia?
•
•
•
•
A.
B.
C.
D.
AVNRT
ORT
Atrial tachycardia
Atrial fibrillation
Answer: AVNRT (A)
• A small R’ is seen is lead V1 with pseudo-S
waves in the inferior leads that are absent
after termination of the arrhythmia. These
represent retrograde atrial activation with a
very short RP interval.
WPW syndrome
• Accelerated AV conduction PR <120 msec
• Prolonged QRS > 120 msec
• Abnormal slurred upstroke of QRS ( delta
wave)
• Abnormal depolarization and repolarization
may lead to pseudoinfarction pattern
WPW pathophysiology
• Short AV conduction
– early excitation of
ventricle at site of
accessory pathway
The result is fusion of both normal and
accessory conduction
No
conduction
• Bizarre upstroke of QRS
delay
– abnormal initial site of
depolarization
• Wide QRS
– early initiation of
ventricular depolarization
AV
node
Accessory
pathway
WPW epidemiology
• Present in 0.3% of the
population
• Risk of sudden death 1 per
1000 patient-years
• Sudden death due to atrial
fibrillation with rapid
ventricular conduction
• Atrial fibrillation often
induced from rapid ORT
ORT(orthodromic
reciprocating tachycardia
Atrial Fibrillation and WPW
• AV nodal blocking
agents may
paradoxically increase
conduction over
accessory pathway by
removing concealed
retrograde penetration
into accessory pathway.
Concealed penetration into the
pathway causes intermittent block
of pathway conduction
Management of Atrial
Fibrillation with WPW
• Avoid AV nodal blockers
• IV procainamide to slow accessory pathway
conduction
• Amiodarone if decreased LVEF
• DC cardioversion if symptomatic with
hypotension
Management of Patients with
WPW
• All patients with symptomatic AF & WPW
should be evaluated with EPS
• Accessory pathways capable of conducting
faster than 240 BPM should be ablated
• Patients with inducible arrhythmias involving
pathway should be ablated
• WPW patients in high risk professions should
be ablated.
A 42 year old smoker presents to the ED with palpitations.
His blood pressure is 100/60. The following rhythm strip
is obtained . What is the next appropriate step?
• A. Emergent cardioversion for polymorphic
VT.
• B. I.V. procainamide
• C. I.V. lidocaine
• D. diltiazem drip to obtain rate control.
Answer B
• This patient has WPW with atrial fibrillation
and a rapid ventricular response. He is stable,
thus I.V. procainamide is indicated to slow
conduction down the accessory pathway.
Diltiazem is contraindicated. Lidocaine will
have no effect, as this is not VT .
Atrial Fibrillation Epidemiology
• Affects 2 to 4% of population
• Increases to 5 to 10 % of patients over 80
• Associated with 2-fold increased risk of
death
• Risk of thromboembolism is approximately
5% per year but may be as high as 20% in
high risk groups not anticoagulated
Mechanism of Atrial Fibrillation
• Multiple reentrant wavelets moving between right
and left atrium
• May be initiated by rapidly firing automatic foci
found commonly in pulmonary veins, SVC, and
coronary sinus.
• Factors that shorten atrial refractoriness and slow
conduction velocity perpetuate atrial fibrillation
• Factors that lengthen atrial refractoriness
(antiarrhythmic drugs ) aid in termination
Management of Atrial Fibrillation
• Aimed at symptom relief by rate and
rhythm control
• Aimed at reducing risk of
thromboembolism by anticoagulation
• Preventing tachycardia mediated
cardiomyopathy (a progressive, reversible
rate-induced form of LV dysfunction)
Acute Management of Atrial
Fibrillation
• Focuses on Rate control
• Patient with atrial fibrillation may undergo DC
cardioversion or pharmacologic conversion if less
than 48 hours duration or following TEE on
Heparin without evidence of left atrial thrombus.
Stroke rate .8%
• Following cardioversion the patient should be kept
anticoagulated for 4 weeks with goal INR of 2 to 3
until atrial function normalizes.
Acute Management of Atrial
Fibrillation
• 50% of patients with paroxysmal atrial
fibrillation will spontaneously convert within
24 hours
• Digoxin used heavily in the past for
prevention and conversion of atrial fibrillation
is ineffective at either and may be
profibrillatory as it decreases the atrial
refractory period
Acute Management of Atrial
Fibrillation
• Rate control may be attained with calcium channel
blockers or beta blockers in patients with normal
L.V. function.
• Calcium channel blockers may be used cautiously in
patients with depressed LV function but are
associated with increased mortality in the long term.
• Beta blockers should be avoided in acutely
decompensated CHF patients with atrial fibrillation
Atrial Fibrillation and Depressed
L.V. Function
• Digoxin and amiodarone may be of effective in
patients with LV dysfunction and
decompensated congestive heart failure to slow
ventricular response.
• Digoxin alone is rarely effective when the
patient is sympathetically driven
• Avoid high dose digoxin with amiodarone as
digoxin levels increase 2-fold with amiodarone
Chronic Management of Atrial
Fibrillation
• Patients with atrial fibrillation, paroxysmal or
sustained should be anticoagulated if any of the
following risk factors for stroke are present:
–
–
–
–
diabetes
valvular disease
hyperthyroidism
Prior CVA
– hypertension
– congestive heart failure
– age greater than 65
Chronic Management of Atrial
Fibrillation
• Rate control with
• Maintenance of sinus
calcium channel
is similar with class I
blockers, beta blockers
and class III drugs
or combination with
approaching 50%
digoxin.
recurrence at 1 year
• Digoxin may be used
• Recurrence of atrial
in bed bound patients
fibrillation 80% at 1
but is easily overcome
year without treatment
with sympathetic
stimulation.
Chronic management of Atrial
Fibrillation
• Class III agents may
have improved
efficacy
– Amiodarone
• pulmonary toxicity
• thyroid
• liver
– Dofetilide
• Torsades des Pointes
– Safe in CHF and CAD
– Limited due to side
effect profile
• Class IC agents safe in
absence of structural
heart disease.
• Few side effects
• Need stress testing
• Can lead to 1 to 1
ventricular conduction
of atrial flutter
• Use with beta blocker
Chronic Management of Atrial
Fibrillation
• Recent large trials reveal no benefit of
rhythm control over rate control.
• Trend of increased mortality in rhythm arm
likely due to proarrhythmia from drugs.
• Patients unable to tolerate atrial fibrillation
due to symptoms were not enrolled in these
studies and are increasingly undergoing
ablation , catheter and surgical procedures.
Nonpharmacologic Treatment of
Atrial Fibrillation
• Maze Procedure
– 90% freedom from atrial
fibrillation
– 2% mortality required
thoracotomy
• Catheter ablation procedure
– only moderate success
– long procedures, difficult
– selecting population
– 60% to 80% effective
– Pulmonary vein
stenosis,cva,perforation,
– esophageal fistula
Nonpharmacologic Treatment of
Atrial Fibrillation
• AV node ablation with pacemaker implant
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–
–
–
recently shown to have no effect on mortality
effective at reducing symptoms
Does not alter need for anticoagulation
Pace at 90 BPM 1 month after procedure to
avoid Torsades des Pointes
Wide ComplexTachycardias
• 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
• SVT with severe hyperkalemia
• SVT with use of antiarrhythmic agents
particularly 1C agents
• SVT with acute MI
Wide-Complex Tachycardia
• Majority are sinus tachycardia with bundle
branch block
• In higher risk population , previous MI,
Decreased Left ventricular dysfunction
– Predominantly Ventricular Tachycardia
Differentiating Ventricular Tachycardia from
SVT with Aberrancy
• Leads to correct initial therapy
• Avoids use of Verapamil which may precipitate
hemodynamic collapse with V.T.
• Cannot use rate or the presence or absence
of symptoms as discriminator !
• Use ECG criteria for diagnosis
• Use presence of risk factors for V.T. as
discriminator
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 Ventricular
Tachycardia
• Clinical condition of patient
– Unstable requires DC cardioversion
– Stable may be treated with Drugs or Cardioversion
• Presence or absence of Left ventricular
Dysfunction determines choice of pharmacologic
therapy
– Amiodarone 150 mg I.V. over 10 minutes may be RX
of choice maximum 2.2 gm/24 hours class IIA
recommendation
New ACLS Algorithm
VT with Depressed Left
Ventricular Function
• Amiodarone is Drug of choice
– mortality neutral or beneficial
– Initial dose 150 mg I.V. over 10 minutes
– effective in Ventricular Fibrillation using 300
mg bolus with improved arrival to hospital.
• DC cardioversion always acceptable option
• Procainamide contraindicated
Ventricular Tachycardia with
Preserved Left Ventricular Function
•
•
•
•
DC cardioversion
Amiodarone 1st line RX according to ACLS
Procainamide
Lidocaine
– Reduced to 3rd line therapy due to relative little
effectiveness in non ischemic VT.
• Avoid use of combination Antiarrhythmic
agents.
Polymorphic VT
• Requires immediate defibrillation as does
VF
• Drug of choice I.V. Lidocaine , Amiodarone
• Usually result of severe metabolic
disturbance or Cardiac ischemia.
• Rarely when associated with prolonged QT
known as Torsades de Pointes
Monomorphic VT in Patients with
Normal Left Ventricular Function
• No structural heart disease
• Present as palpitations, syncope but rarely as sudden
death
• Right ventricular outflow tachycardia
– LBB morphology inferior axis
– adenosine, Calcium channel , occ beta blockers
– Amenable to Ablation
• Idiopathic Left ventricular tachycardia
– RBB superior axis Verapamil and adenosine
sensitive
– Amenable to Ablation
Torsades de Pointes
• Polymorphic VT associated with long QT
– increased risk if QTC 500 msec or greater QT >
600 msec.
• Frequently initiated after pause
• Usually Iatrogenic
– Hypokalemia,Hypomagnesemia, Drugs,
combination
• May be congenital
– LQT1, LQT2,LQT3
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
•
•
•
•
Remove Offending Agent
Replete Potassium
Treat with Magnesium even if normal
Consider increasing heart rate
– isoproterenol
– Pacing
• Treat Congenital with Beta blockers and
Pacing or ICD
Sudden Death with Normal Left
Ventricular Function
• Brugada Syndrome
– Incompete RBB ST elevation V1V2
– exacerbated by Procainamide and Flecainide
– ICD implantation
• Right ventricular Dysplasia
– Delayed Right Ventricular activation
– Epsilon wave , deep precordial Twave inversion
– fatty infiltration RV, MRI, RV gram
Sudden Death with Normal Left
Ventricular Function
• Hypertrophic Cardiomyopathy
– Majority of sudden death in U.S. in young
patients without coronary artery disease
– Risk factors extreme hypertrophy(>3.0
cm)exertional hypotension, nonsustained
VT,syncope, family history sudden death
– ICD effective but appropriate selection for
primary prevention problematic
Sudden Death with Normal Left
Ventricular Function
• Brugada Syndrome
– Incompete RBB ST elevation V1V2
– exacerbated by Procainamide and Flecainide
– ICD implantation
• Right ventricular Dysplasia
– Delayed Right Ventricular activation
– Epsilon wave , deep precordial Twave inversion
– fatty infiltration RV, MRI, RV gram
Implantable Cardiodefibrillator
• Superior to Drug therapy in patients with
sudden death and coronary disease
• Reduced risk of death in patients with
sudden death coronary disease and EF
<35% over drugs
• Reduces risk of death in patients with
inducible VT and reduced L.V. fxn and
CAD by nearly 50%
Reductions in Mortality with ICDs
Compared to Antiarrhythmic Drugs
% Mortality Reduction
60%
54%
50%
37%
40%
31%
30%
20%
20%
10%
0%
1
AVID1
CASH2
CIDS3
MADIT4
3 years
2 years
3 years
2 years
The AVID Investigators. N Engl J Med. 1997;337:1576-1583.
2 Kuck K. ACC98 News Online. April, 1998. Press release.
3
Connolly S. ACC98 News Online. April, 1998. Press release.
AJ. N Engl J Med. 1996;335:1933-1940.
4 Moss
SCD-Heft
Patients with class II,III CHF EF
<35%
34.1%
40
35.8%
35
28.9%
30
25
ICD
Amiodarone
Placebo
20
15
10
5
0
Mortality at 5 years
Conclusion
• Most Arrhythmias are reentry
• Unstable patient should undergo DC
cardioversion, or defibrillation
• Class I agents should be avoided in patients
with structural heart disease
• Amiodarone is drug of choice with
depressed left ventricular function
Conclusion
• Atrial Fibrillation may be treated with rate
or rhythm control
• WPW patients should be screened for
symptoms.If asymptomatic no further
evaluation is generally needed.
• WPW patients with symptoms or able to
conduct faster than 240 BPM should be
ablated
A 67 year old male with history of previous infarct and
reduced LV function presents with palpitations and dizziness.
His blood pressure is 80/40. The appropriate next step is ?
• A. Synchronized cardioversion for VT
• B. I.V. Procainamide for Atrial Fibrillation
with WPW syndrome
• C. Synchronized cardioversion for unstable
SVT with aberrancy.
• D. I.V. Amiodarone for SVT with aberrancy
in a patient with reduced LV function.
Answer A.
• This patient has ventricular tachycardia. An
RS interval of greater than 100 msec is
clearly visible. In addition, by history this
patient is overwhelmingly likely to present
with VT with a wide complex rhythm. Also
this patient is not stable with relative
hypotension requiring immediate
cardioversion as opposed to pharmacologic
therapy.
A 24 year old male is referred to you for evaluation
due to an unusual ECG. He has never had any
palpitations, syncope or near-syncope. Appropriate
next step would be which of the following?
• A. Immediate for referral for ICD implant
• B. Reassurance that no further evaluation is
needed at this time
• C. Referral for EPS and catheter ablation of
his accessory pathway.
• D. Send him to someone who knows what
this is.
Answer B
• This patient does indeed have an accessory
pathway. However he demonstrates
intermittent pre-excitation at a slow rate
which places him in a low risk group.Without
symptoms, no further evaluation is needed.
Every other beat in the ECG is pre-excited.
You are called to assess a patient in the SICU for
unexplained tachycardia . Which of the following is
most correct?
• A. The treatment depends on how long the
patient has been in this rhythm
• B. No treatment is needed as the patient is
in sinus tachycardia.
• C. Immediate cardioversion should be
performed regardless of the rhythm.
• D. Adenosine will likely terminate this
arrhythmia.
Answer A.
• This patient is in atrial flutter with variable
ventricular response. Flutter waves are
intermittently visible on ECG tracing when higher
AV block is seen. In addition, flutter waves are
visible on the CVP pressure tracing also defining
the rhythm. Cardioversion would be inappropriate
if the patient had been in this rhythm greater than
48 hours without first performing a TEE given the
risk of thromboembolism.
A 46 year old female is admitted with dizziness. She is
an alcoholic, on methadone, with schizophrenia. She
began feeling dizzy after starting a fluoroquinalone for a
UTI. Which of the following should be your next step?
• A. Administer I.V . Procainamide
• B. Consult E.P. for placement of a defibrillator
• C. Discontinue antibiotic, treat with I.V.
magnesium, discontinue antipsychotic, and
consider temporary pacing
• D. Administer I.V. amiodarone because it is unlikely
cause Torsades de Pointes.
Answer C.
• This patient has Torsades de Pointes with
classic polymorphic VT and prolonged QT
demonstrated in the bottom strip.
Antipsychotics, hypomagnesemia,
quinolones all may predispose to this
arrhythmia. Procainamide or amiodarone
would worsen this rhythm. ICD is not
indicated .