1. Tachyarrhythmias, Diagnosis and Management
Laurent Lewkowiez, MD
Assistant Professor
Denver Health and Hospitals
University of Colorado Health Sciences

2. 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

3. Reentry Most common mechanism
Requires two separate paths of conduction
Requires an area of slow conduction
Requires unidirectional block

4. Supraventricular Tachycardias Diagnosis
ECG is cornerstone
Observe zones of transition for clues as to mechanism:
onset
termination
slowing, AV nodal block
bundle branch block

5. 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

6. 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

7. 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

8. 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

9. Ablation AVNRT
His bundle
Ablation area

10. 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

11. 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

12. 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

13. 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.

14. 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.

15. 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

16. 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%

17. 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

18. 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

19. Atrial Flutter

20. 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.

21. A. AVNRT B. ORT C. Atrial tachycardia D. 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. AVNRT
B. ORT
C. Atrial tachycardia
D. Atrial fibrillation

24. 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.

25. 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

26. WPW pathophysiology Short AV conduction Bizarre upstroke of QRS
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

27. 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

28. 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

29. 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

30. 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.

31. A. Emergent cardioversion for polymorphic VT. B. I.V. procainamide
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.

33. 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 .

34. 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

35. 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

36. 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)

37. 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.

38. 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

39. 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

40. 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

41. 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

42. 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

43. 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

44. 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.

45. 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

46. 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

47. Wide ComplexTachycardias
Ventricular Tachycardia
SVT with aberrancy (functional bundle branch block)
SVT with underlying bundle branch block
SVT with pre-excitation

48. Additional Mimimics of Wide Complex Tachycardias
SVT with severe hyperkalemia
SVT with use of antiarrhythmic agents particularly 1C agents
SVT with acute MI

49. Wide-Complex Tachycardia
Majority are sinus tachycardia with bundle branch block
In higher risk population , previous MI, Decreased Left ventricular dysfunction
Predominantly Ventricular Tachycardia

50. 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

51. The Brugada Criteria

52. Morphology Criteria for VT

53. 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

54. New ACLS Algorithm

55. 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

56. 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.

57. 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

58. 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

59. 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

61. 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

62. 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

63. 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

64. 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

65. 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%

66. Reductions in Mortality with ICDs Compared to Antiarrhythmic Drugs3 7 % 2 5 4 1 6
% Mortality Reduction
Reductions in mortality with ICDs vs. drugs:
VT/VF Patients
1 AVID: 31% at 3 years and 39% at 1 year (ICD versus empiric amiodarone or sotalol)
2 CASH: 37% at 2 years (ICD versus amiodarone, metoprolol or propafenone)
3 CIDS: 20% at 3 years (ICD versus amiodarone)
Post-MI Patients
4 MADIT: 54% at 2 years (ICDs versus conventional treatment – mostly amiodarone)
AVID1
3 years
CASH2
2 years
CIDS3
3 years
MADIT4
2 years
1 The AVID Investigators. N Engl J Med. 1997;337:
2 Kuck K. ACC98 News Online. April, Press release.
3 Connolly S. ACC98 News Online. April, Press release.
4 Moss AJ. N Engl J Med. 1996;335:

67. SCD-Heft Patients with class II,III CHF EF <35%
34.1%
35.8%
28.9%

68. 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

69. 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

70. A. Synchronized cardioversion for VT
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.

72. 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.

73. A. Immediate for referral for ICD implant
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.

75. 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.

76. B. No treatment is needed as the patient is in sinus tachycardia.
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.

78. 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.

79. A 46 year old female is admitted with dizziness
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.

81. 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 .