1. Lisa Campfens MD, FRCPC, FACEP
Tachydysrrhythmias
Lisa Campfens MD, FRCPC, FACEP

2. Generation of Dysrrhythmias
Two fundamental causes
Disturbances of automaticity
Disturbances of conduction
AV block
Reentry
Abnormal electrical activity in heart
Too fast/too slow
Supraventricular vs ventricular

3. Presentation Multiple symptoms:
Fatigue Chest pain
Dyspnea Dizziness
Presyncope Palpitations
Patients can be symptomatic even with single premature beats or non-sustained atrial arrhythmias
Chest pain usually unrelated to CAD

4. Complications 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
Rapid stimulation of atrial tissue occurs at bpm> mean of 170bpm
Persistence of tachycardia: decreased cardiac output
increased CHF
increased ischemia
Usually takes weeks to months to develop
Ventricular dysfx usually reversable

5. Referral All patients with wide complex tachycardia of unknown origin
Resistant/intolerant to pharmacological therapy
WPW Syndrome

6. Classification of Antidysrrhythmic Drugs
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

7. Class I: Na Channel Blockers
Class IA Quinidine, Procainamide
Class IB Lidocaine, Phenytoin, Mexilitine
Class IC Flecainide, Propafenone
All class IC agents can exacerbate existing dysrhythmias and create new ones

8. Procainamide Therapeutic use Ventricular tachycardia
SVT with aberrancy
Pre-excitation Syndromes
Old drug/ now for most part replaced by Amiodarone as first line agent for chemical cardioversion. There has not been any head to head comparison of the two drugs
After use of procainamide, in most cases still need to put the patient on a long-term oral agent
Both Procainamide and Amiodarone prolong QT- contraindicated in Torsades de pointes
Adverse effects: hypotension

9. Class II: Beta Blockers
Metoprolol, Atenolol, Esmolol
Therapeutic use
Slow ventricular rate (A fib/ A flutter)
Terminate SVT caused by an AV nodal reentrant circuit
Meotprolol: 5mg IV for 3 doses q2-5min

10. Class II: Beta Blockers (cont’d)
Adverse effects
Heart block
Heart failure
AV block
Sinus arrest
Hypotension
Bronchospasm (asthma/COPD)

11. Class III: K Channel Blockers
Amiodarone
Therapeutic use
Life-threatening ventricular dysrrhythmias
SVT with aberrancy
Pre-excitation Syndromes
QRS widening
Prolongation of the PR and QT intervals
150mg IV over 10 mins then 1mg/min for 6 hours

12. 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
Ist choice if contraindication to B blocker or if Adenosine terminates PSVT but recurs immediately
Diltiazem: 0.25mg/kg IV, may repeat at 0.35mg/kg in 15 mins
Verapamil: 5-10mg IV, may repeat to max 15mg .

13. Other Antidysrhythmic Drugs
Adenosine
Half-life few seconds
Intense but transient AV block thereby terminating tachycardia
Safe in patients with heart disease
Contraindications: asthma/COPD
Therapeutic use
termination of PSVT
Should also theoretically be avoided in wide QRS tachycardia. If given to WPW with AF could detiorate into VF

14. PSVTs A Fibrillation A Flutter AVNRT AVRT (ORT)
SVT includes all forms of tachycardia that arise above the bifurcation of the bundle of HIS
HR at least 100bpm
QRS usually narrow
Tachys which respond to vagal maneuvers or other cholinergic agents like adenosine are usually due to re-entry and involve the compact region of the AV node
SVT that persists even when AV block is achieved by CSM or other interventions are independent of AVN conduction
QRS maybe widened /abnormal because of intrinsic conduction disturbance, myocardial disease, or rate-related BBBB.
Rate-related BBB: occurs if either right or keft BB reaches its effective refractory period and cannot conduct impulses to match the rapid rate of the tachycardia

15. Reentry Most common mechanism
Requires two separate paths of conduction
Requires an area of slow conduction
Requires unidirectional block 15

16. Regular SVT in Adults 90% reentrant 60% AVNRT 30% AVRT (ORT)
10% Atrial tachycardia
2 to 5% involve WPW syndrome 16

17. AV Nodal Reentrant Tachycardia
Slow pathway
Re-entrant circuit is small and is in or closely related to the AV node
Re-entrant circuit is small and is in or closely related to the AV node
Narrow QRS
Absent p waves
Rate bpm
Fast pathway 17

18. AV Nodal Reentrant Tachycardia
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 18

19. Orthodromic Reciprocating Tachycardia
Conduction down AVnode
Anterograde over AV node and retrograde conduction of an accessory pathway.
Frequently presents in patients with WPW as narrow complex tachycardia
Up accessory pathway
AVRT(ORT): re-entrant circuit large-involves atria, AV node and ventricles
QRS narrow 19

20. 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 20

21. Atrial Tachycardia Atrial rate 150-250 bpm
Does not require AVN or infranodal conduction
P wave morphology different
PR interval > 120 ms differentiating from junctional tachycardia
Origin inferred from P wave morphology. 21

22. Atrial Tachycardia
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.
Adenosine may help with diagnosis if AV block occurs and continued arrhythmia likely atrial tachycardia 22

23. Atrial Tachycardia
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 23

24. Atrial Tachycardia Therapy
Antiarrhythmics
Class 1 : procainamide, quinidine, flecainide Patients without structural heart disease.
Class III : sotalol, amiodarone, dofetilide
AVN blocking agents for rate control
Catheter ablation effective in 70-80% 24

25. 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
Rapid atrial depolarization of bpm
Block can be variable and appear as irregular
Often converts to AF or NSR
Re-entrant circuit confined to right atrium
Sync cardioversion start at 25J
Antiarrhythmic drugs not very successful-50% 25

26. 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 26

27. 42 year old smoker presents to the ED with palpitations. BP 100/60.
A. Emergent cardioversion for polymorphic VT
B. IV procainamide
C. IV lidocaine
D. IV diltiazem to obtain rate control. 27

28. 28

29. Answer
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
Ca channel blockers block AV node and accelerate conduction down accessory pathway thaT HAS VERY SHORT REFRACTION PERIOD THEREFORE allowing AF to detiorate to VF very quickly. Results in refractory hypotension and refractory to cardioversion 29

30. Epidemiology of AF 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
Most common arrhythmia encountered
15-25% of all strokes in US can be attributed to AF
Random chaotic depolarization of atria bpm but ventricular rate limited by refractory period of AVN so ventricular rate bpm
Irregularly irregular 30

31. Management of Atrial Fibrillation
Symptom relief by rate and rhythm control
Reduce risk of thromboembolism by anticoagulation
Prevent tachycardia-mediated cardiomyopathy 31

32. Acute Management of AF Focus on rate control
DC cardioversion or pharmacologic conversion if <48 hrs or following TEE on Heparin without evidence of left atrial thrombus
Following cardioversion anticoagulate for 4 wks with goal INR of 2-3 until atrial fx normalizes**
. Stroke rate .8%
Amiodarone is a lousy rate control agent. Often combine with B blocker to slow rate and then Amiodarone to cardiovert over time
Stunning of atria and stasis can occur after cardioversion leading to thrombus formation even though patient in NSR
Patients often unaware of short episodes of AF 32

33. Acute Management of AF 50% spontaneously convert <24 hours
Digoxin used heavily in past for prevention/ conversion, ineffective at either
May be profibrillatory as decreases atrial refractory period 33

34. Acute Management of Atrial Fibrillation
Rate control: Ca channel blockers or B blockers in patients with normal LV fx
Cautious use of Ca channel blockers if depressed LV fx. Associated with increased mortality in long term.
Avoid Beta blockers in acutely decompensated CHF patients with AF 34

35. AF and Depressed LV Fx
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 35

36. Chronic Management of AF
Maintenance of sinus similar with class I and class III drugs-50% recurrence at 1 year
Recurrence of AF 80% at 1 year without treatment 36

37. Chronic Management of AF
Recent large trials reveal no benefit of rhythm vs rate control
Trend of increased mortality in rhythm arm
Patients unable to tolerate AF due to symptoms were not enrolled in these studies and are increasingly undergoing ablation , catheter and surgical procedures.
Trend of increased mortality in rhythm arm likely due to pro-arrhythmia from drugs 37

38. Wide ComplexTachycardias
Ventricular Tachycardia
SVT with aberrancy (functional bundle branch block)
SVT with underlying bundle branch block
SVT with pre-excitation 38

39. Additional Mimimics of Wide Complex Tachycardias
SVT with severe hyperkalemia
SVT with use of antiarrhythmic agents particularly 1C agents
SVT with acute MI 39

40. Wide-Complex Tachycardia
Majority are SVT with BBB
In higher risk population VT until proven otherwise
:High risk:
Most important predictor of VT is prev MI with centricular myocardial scar formation
LV dysfx
Valvular HD
Congenital HD 40

41. Differentiating VT from SVT with Aberrancy
Leads to correct initial therapy
Verapamil may ppt hemodynamic collapse
Hemodynamic status or rate not a clue to mechanism
In higher risk population VT until proven otherwise
ECG criteria for diagnosis
V tach: repetetive firing of an irritable ventricular ectopic focus at bpm
V fib: electricaL CHAOS IN VENTRICLES
Avoids use of Verapamil which may precipitate hemodynamic collapse refractory hypotension/refractory to cardioversion 41

42. The Brugada Criteria Clinical signs of AV dissociation: Cannon a waves
Irregular pulse
Varying intensity of S1
Beat to beat change in SBP
ECG signs of Av dissociation:
Pathopneumonic for V tach but only seen in 25%
Independent P waves
Capture/fusion beats
Capture: when sinus impulse conducted to ventricle during VT
Fusion: sinus impulse activates the ventricle at the same time as a VPC (leads to narrower QRS complexes)
Indeterminate axis/ extreme right axis
Uniform concordance In V1-V6 either positive or negative 42

43. Morphology Criteria for VT43

44. Therapy for VT Stable-chemical or DC cardioversion
Unstable-DC cardioversion
Amiodarone 150 mg IV over 10 mins, max 2.2 gm/24 hrs class IIA recommendation 44

45. New ACLS Algorithm

46. VT with Depressed LV Fx 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.
DC cardioversion always acceptable option
Procainamide contraindicated 46

47. VT with Preserved LV Fx DC cardioversion
Amiodarone 1st line RX according to ACLS
Procainamide
Lidocaine
Avoid use of combination antiarrhythmic agents
Lidocaine: Reduced to 3rd line therapy due to relative little effectiveness in non ischemic VT. 47

48. AVRT Extranodal Accessory Pathways and WPW Syndrome
Extremely symptomatic but rarely observed
In the presence of AF, VF can occur if the refractory period of the accessory pathway is <250 msec
WPW syndrome is reserved for those persons who have a combination of the WPW pattern and SVT.

49. WPW Not an arrhythmia but a clinical syndrome
ECG: PR<.12 sec, QRS>.10 sec, delta wave
Many types of arrhythmias
‘Is AVN an integral part or an innocent bystander?’
Syndrome: predilection for dysrrythmias
abn ECG
symptoms
Pre-excitation: implies early depolarization of ventricle represented as delta wave
Delta wave- dec PR in association with slurring of upstroke of QRS.
PR is short because ventricle being prematurely activated through accessory path
QRS wide because ventricle activated from abn location
Sinus impulse travels to ventricle via both AV node and accessory pathways. Results in fusion of ventricular activity via both conventional His-Purkinje system and the accessory path
Because AV nodal conduction is decremental and relatively slow, the 1st part of the QRS is slurres. Anterograde accessory pathway conduction reaches ventricle 1st forming delta wave. This slurring persists until AV node conduction propagates into ventricle, activating ventricle rapidly and resulting in terminal QRS that is closer to normal in morphology
Abn ECG not always present(depends on tone of AVN, location of accessory path, site of atrial impulse, size of atria, etc)

50. WPW AV Node Integral AVRT-Orthodromic AVRT-Antidromic
AV blocking diagnostic and therapeutic
AVRT-Antidromic
Regular
AVRT-Orthodromic
Most common type
PAC conducts down AVN and up accessory path
Narrow QRS, regular, occ neg P
AVRT-Antidromic
Conduction down accessory path and retrograde through AVN
Wide QRS

51. WPW AV Node Innocent Bystander AF Can be serious problem
Normal AVN protects ventricle from fast atrial rate in AF. If refractory period of accessory path is short, may allow rapid activation of ventricle ( bpm) ie VF

52. Polymorphic VT Immediate defibrillation IV Lidocaine , Amiodarone
Usually result of severe metabolic disturbance or cardiac ischemia.
Important to differentiate polymorphic VT form Torsades.
Normal QT
Important implications for treatment 52

53. Monomorphic VT in Patients with Normal LV Fx
No structural heart disease
Present as palpitations, syncope but rarely as sudden death 53

54. Monomorphic VT in Patients with Normal LV Fx
RV outflow tachycardia
LBB morphology inferior axis
adenosine, Calcium channel , occ beta blockers
Amenable to Ablation
Idiopathic LV tachycardia
RBB superior axis
Verapamil and adenosine sensitive

55. Torsades de Pointes Polymorphic VT assoc with long QT
QTc >440msec , QT > 500 msec
Frequently initiated after pause
Iatrogenic
hypoK, hypoMg, Hypo Ca, Drugs, Combination
Congenital
V rate >200bpm
Undulating axis- polarity of complexes shift about baseline
Usually short episodes<20secs but sustained runs can be seen
Prolonged QT during sinus rhythm
Electrophysiologic mechs not well understood. Current research has focused on ‘early after-depolarizations’
Iatrogenic-
Drugs: Anti-arhrythmics-Class 1a,1c III
Anti-psychotics-phenothiazines, haloperidol
Anti-depressants-TCAs
Antibiotics
Anti-histamines
Combo of Quinidine, Digoxn and hypo K well documented
Metabolic: hypoK,Mg,Ca
CNS: SAH, ICH, tumor
CARDIAC: ischemia
myocarditis
severe bradyarrhythmias
TOXINS: organophosphates
HYPOTHYROIDISM 55

56. Drug-induced Torsades is an idiosyncratic response unrelated to drug level. Usually seen within 7 days of initiation of therapy. Can occur without reliable warning signs
Anti-arhrythmics-Class 1a,1c III
Anti-psychotics-phenothiazines, haloperidol
Anti-depressants-TCAs
Antibiotics
Anti-histamines
Combo of Quinidine, Digoxn and hypo K well documented 56

57. Treatment of Torsades de Pointes
Goal to shorten QT
Remove offending agent
Replete K
IV Mg even if normal level
Mg tx of choice. Mech of action unclear. Does not shorten QT. Mg levels often normal pre-initiation
2g bolus over 15-20mins and repeat prn twice. IV drip 3-20mg/min
Treat Congenital with B blockers and Pacing or ICD 57

58. Treatment of Torsades de Pointes
Overdrive pacing
isoproterenol
Pacing
DC Cardioversion
Rarely required
May be refractory

59. Sudden Death with Normal LV Fx
Brugada Syndrome
Incompete RBB ST elevation V1V2
RV Dysplasia
Delayed RV activation
Epsilon wave , deep precordial Twave inversion
Brugada Syndrome
Incompete RBB ST elevation V1V2
No structural heart disease
Genetic
Normal QTc
exacerbated by Procainamide and Flecainide
ICD implantation
Prone to develop Torsades and VF leading to sudden cardiac death
RV Dysplasia
Delayed RV activation
Epsilon wave , deep precordial Twave inversion
fatty infiltration RV, MRI, RV gram 59

60. Sudden Death with Normal LV FX
Hypertrophic Cardiomyopathy
Major cause in U.S. in young patients without CAD
Risk factors
ICD effective
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 60

61. A. Synchronized cardioversion for VT
67 yr old male with prior infarct and LV dysfx presents with palpitations and dizziness. BP is 80/40
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 61

62. 62

63. Answer
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. 63

64. A. Administer IV Procainamide B. Consult EP for placement of a ICD
46 yr old alcoholic, on methadone, with schizophrenia. She began feeling dizzy after starting a fluoroquinalone for a UTI
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 64

65. 65

66. Answer
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 .
Antipsychotics, hypoMg, quinolones, all may predispose to this arrhythmia. 66