Tachyarrhythmias, Diagnosis and Management

1
Tachyarrhythmias, Diagnosis and Management

• Laurent Lewkowiez, MD
• Assistant Professor
• Denver Health and Hospitals
• University of Colorado Health Sciences

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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

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Reentry

• Most common mechanism
• Requires two separate paths of conduction
• Requires an area of slow conduction
• Requires unidirectional block

4
Supraventricular TachycardiasDiagnosis

• ECG is cornerstone
• Observe zones of transition for clues as to
  mechanism
• onset
• termination
• slowing, AV nodal block
• bundle branch block

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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

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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
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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
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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

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Ablation AVNRT
His bundle
Ablation area
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Orthodromic Reciprocating Tachycardia
Conduction down AVnode

• 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

Up accessory pathway
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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
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Differential Dx of Regular SVT
Long RP interval

• Long RP tachycardia
• Atrial tachycardia
• Sinus node reentry
• Sinus tachycardia
• Atypical AV nodal reentrant tachycardia
• Permanent form of junctional reciprocating
  tachycardia

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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 gt 120 msec differentiating from
  junctional tachycardia
• Origin inferred from P wave morphology.

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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.

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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

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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

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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

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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

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Atrial Flutter
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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.

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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. AVNRT
• B. ORT
• C. Atrial tachycardia
• D. Atrial fibrillation

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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.

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WPW syndrome

• Accelerated AV conduction PR lt120 msec
• Prolonged QRS gt 120 msec
• Abnormal slurred upstroke of QRS ( delta wave)
• Abnormal depolarization and repolarization may
  lead to pseudoinfarction pattern

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WPW pathophysiology

• Short AV conduction
• early excitation of ventricle at site of
  accessory pathway
• Bizarre upstroke of QRS
• abnormal initial site of depolarization
• Wide QRS
• early initiation of ventricular depolarization

The result is fusion of both normal and accessory
conduction
No conduction delay
AV node
Accessory pathway
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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
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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
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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

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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.

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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.

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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 .

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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

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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

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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)

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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.

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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

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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

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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

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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 hypertension
• valvular disease congestive heart failure
• hyperthyroidism age greater than 65
• Prior CVA

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Chronic Management of Atrial Fibrillation

• Rate control with calcium channel blockers, beta
  blockers or combination with digoxin.
• Digoxin may be used in bed bound patients but is
  easily overcome with sympathetic stimulation.

• Maintenance of sinus is similar with class I and
  class III drugs approaching 50 recurrence at 1
  year
• Recurrence of atrial fibrillation 80 at 1 year
  without treatment

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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

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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.

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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

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Nonpharmacologic Treatment of Atrial Fibrillation

• AV node ablation with pacemaker implant
• 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

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Wide ComplexTachycardias

• Ventricular Tachycardia
• SVT with aberrancy (functional bundle branch
  block)
• SVT with underlying bundle branch block
• SVT with pre-excitation

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Additional Mimimics of Wide Complex Tachycardias

• SVT with severe hyperkalemia
• SVT with use of antiarrhythmic agents
  particularly 1C agents
• SVT with acute MI

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Wide-Complex Tachycardia

• Majority are sinus tachycardia with bundle branch
  block
• In higher risk population , previous MI,
  Decreased Left ventricular dysfunction
• Predominantly Ventricular Tachycardia

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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

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The Brugada Criteria
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Morphology Criteria for VT
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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

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New ACLS Algorithm
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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

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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.

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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

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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

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Torsades de Pointes

• Polymorphic VT associated with long QT
• increased risk if QTC 500 msec or greater QT gt
  600 msec.
• Frequently initiated after pause
• Usually Iatrogenic
• Hypokalemia,Hypomagnesemia, Drugs, combination
• May be congenital
• LQT1, LQT2,LQT3

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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

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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

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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(gt3.0
  cm)exertional hypotension, nonsustained
  VT,syncope, family history sudden death
• ICD effective but appropriate selection for
  primary prevention problematic

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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

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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 lt35 over drugs
• Reduces risk of death in patients with inducible
  VT and reduced L.V. fxn and CAD by nearly 50

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Reductions in Mortality with ICDsCompared to
Antiarrhythmic Drugs
Mortality Reduction
AVID1 3 years
CASH2 2 years
CIDS3 3 years
MADIT4 2 years
1 The AVID Investigators. N Engl J Med.
19973371576-1583. 2 Kuck K. ACC98 News Online.
April, 1998. Press release.
3 Connolly S. ACC98 News Online. April, 1998.
Press release. 4 Moss AJ. N Engl J Med.
19963351933-1940.
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SCD-HeftPatients with class II,III CHF EF lt35
34.1
35.8
28.9
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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

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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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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 .