1. Fundamentals and what you should know for the big, bad BOARDS!
Arrhythmias 101
Fundamentals and what you should know for the big, bad BOARDS!

2. The Basics
SA Node and AV node cells are slow conductors activated by calcium, thus blocked by calcium channel blockers such as verapamil
Atrium, Bundle of His, and ventricle cells are fast conducting and activated by sodium, thus blocked by sodium channel blockers (class 1 anti-arrhythmics) such as quinidine, lidocaine and propafenone.
First, the basics…

3. 4 Mechanisms of Arrhythmia
reentry (most common)
automaticity
parasystole
triggered activity

4. Cardiac Conduction Tissue
Reentry Requires…
Electrical Impulse
Cardiac Conduction Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
2 distinct pathways that come together at beginning and end to form a loop.
A unidirectional block in one of those pathways.
Slow conduction in the unblocked pathway.

5. Cardiac Conduction Tissue
Reentry Mechanism
Premature Beat Impulse
Cardiac Conduction Tissue
Repolarizing Tissue (long refractory period)
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
1. An arrhythmia is triggered by a premature beat
2. The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway

6. Cardiac Conduction Tissue
Reentry Mechanism
Cardiac Conduction Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
3. The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway

7. Cardiac Conduction Tissue
Reentry Mechanism
Cardiac Conduction Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
4. On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit

8. Reentry Circuits AV Nodal Reentry SVT Ventricular Re-entry
ventricular tachycardia
Atrial Reentry
atrial tachycardia
atrial fibrillation
atrial flutter
SA Node
Atrio-Ventricular Reentry
WPW
SVT

9. Reentry Requires…
2 distinct pathways that come together at beginning and end to form a loop.
A unidirectional block in one of those pathways.
Slow conduction in the unblocked pathway.
Large reentry circuits, like a-flutter, involve the atrium.
Reentry in WPW involves atrium, AV node, ventricle and accessory pathways.
Large reentry circuits, like a-flutter, involve the atrium.
Reentry in WPW involves atrium, AV node, ventricle and accessory pathways.

10. Automaticity
Heart cells other than those of the SA node depolarize faster than SA node cells, and take control as the cardiac pacemaker.
Factors that enhance automaticity include:
 SANS,  PANS,  CO2,  O2,  H+,  stretch, hypokalemia and hypocalcaemia.
Examples: Ectopic atrial tachycardia or multifocal tachycardia in patients with chronic lung disease OR ventricular ectopy after MI

11. Parasystole…
is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells.
3% of PVCs

12. Triggered activity…
is like a domino effect where the arrhythmia is due to the preceding beat.
Delayed after-depolarizations arise during the resting phase of the last beat and may be the cause of digitalis-induced arrhythmias.
Early after-depolarizations arise during the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced)

13. What tools to use and when to use it…
Diagnosis…
What tools to use and when to use it…

14. Event Monitors
Holter monitoring: Document symptomatic and asymptomatic arrhythmias over hours. Can also evaluate treatment effectiveness in a-fib, pacemaker effectiveness and identify silent MIs.
Trans-telephonic event recording: patient either wears monitor for several days or attaches it during symptomatic events and an ECG is recorded and transmitted for evaluation via telephone. Only 20% are positive, but still helpful.

15. Exercise testing Symptoms only appear or worsen with exercise.
Also used to evaluate medication effectiveness (esp. flecanide & propafenone)
 You can assess SA node function with exercise testing.
 Mobitz 1 (Wenkebach) is blockage at the AV node, so catecholamines from exercise actually help!
 Mobitz 2 is blockage at bundle of His, so it worsens as catecholamines from exercise increase AV node conduction, thus prognosis is worse.
*PVCs occur in 10% without and 60% of patients with CAD. *PVCs DO NOT predict severity of CAD (neither for nor against)!

16. Signal Averaged ECG
Used only in people post MI to evaluate risk for v-fib or v-tach.
Damage around the infarct is variable, so this measures late potentials (low-signal, delayed action potentials) as they pass through damaged areas.
Positive predictive value is 25%-50% but negative predictive value is 90%-95%, thus if test is negative, patient is at low risk.

17. Electrophysiologic Testing…
Catheters are placed in RA, AV node, Bundle of HIS, right ventricle, and coronary sinus (to monitor LA and LV).
Used to evaluate cardiogenic syncope of unknown origin, symptomatic SVT, symptomatic WPW, and sustained v-tach.
*Ablative therapy is beneficial in AV node reentry, WPW, atrial tachycardia, a-flutter, and some v-tach. Complication is 1%

18. The slow pokes (HR<60)…
Bradyarrhythmias
The slow pokes (HR<60)…

19. Sick Sinus Syndrome
Conduction problem with no junctional escape during sinus pause
Diagnose with ECG or Holter. If inconclusive, need electrophysiologic testing.
If asymptomatic, leave alone. If symptomatic, needs pacemaker.

20. First Degree AV Block
Delay at the AV node results in prolonged PR interval
PR interval>0.2 sec.
Leave it alone

21. Second Degree AV Block Type 1 (Wenckebach)
Increasing delay at AV node until a p wave is not conducted.
Often comes post inferior MI with AV node ischemia
Gradual prolongation of the PR interval before a skipped QRS. QRS are normal!
No pacing as long as no bradycardia.

22. Second Degree AV Block Type 2
Diseased bundle of HIS with BBB.
Sudden loss of a QRS wave because p wave was not transmitted beyond AV node. QRS are abnormal!
May be precursor to complete heart block and needs pacing.

23. Third Degree AV Block Must treat with pacemaker.
Complete heart block where atria and ventricles beat independently AND atria beat faster than ventricles.
Must treat with pacemaker.

24. LBBB

25. Left Bundle Branch Block
Left ventricle gets a delayed impulse
QRS is widened (at least 3 boxes)
V5 and V6 have RR’ (rabbit ears)
Be careful not to miss any hiding q waves!
Pacemaker if syncope occurs

26. Right Bundle Branch Block

27. Right Bundle Branch Block
Right ventricle gets a delayed impulse
QRS is widened (at least 3 boxes)
V1 and V2 have rSR’
Pacemaker if syncope occurs.

28. Bifascicular Block QRS is widened (at least 3 boxes)
RBBB plus LABB OR RBBB plus LPBB
QRS is widened (at least 3 boxes)
V5 and V6 have RR’ (rabbit ears)
V1 and V2 have rSR’
Pacemaker if syncope occurs

29. The speed demons…(HR >100)
Tachyarrhythmias
The speed demons…(HR >100)

30. Tachyarrhythmias Supraventricular tachycardia Atrial fibrillation
Atrial flutter
Ventricular tachycardia
Monomorphic
Polymorphic (Torsades de pointe)
Ventricular fibrillation

31. Supraventricular Tachycardia

32. SVT Reentrant arrhythmia at AV node that is spontaneous in onset
May have neck fullness, hypotension and/or polyuria due to ANP
Narrow QRS with tachycardia
First line is vagal maneuvers
Second line is adenosine or verapamil
For chronic SVT, class 1A or 1C or amiodarone or sotalol work well
Ablation will cure it too, but we usually do this only in young patients

33. Multifocal Atrial Tachycardia

34. MAT Automatic atrial rhythm from various different foci
Seen in hypoxia, COPD, atrial stretch and local metabolic imbalance.
Three or more types of p waves and a rate > 100
Digoxin worsens it, so treat with oxygen and slow channel blocker like verapamil or diltiazem.

35. Wolf Parkinson White

36. WPW
Ventricles receive partial signal normally and partially through accessory pathway
Symptomatic tachycardia, short PR interval (<0.12), a delta wave and prolonged QRS (>0.12)
Electrophysiologic testing helps to identify the reentry pathway and location of the accessory pathway

37. WPW
Because WPW has both normal conduction through the AV node and accessory pathway conduction that bypasses the AV node, a-fib can happen via the accessory pathway
Inhibition of the AV node will end up in worsening the a-fib because none of the signals are slowed down by the AV node before hitting the ventricle.
* Do not use any meds that will slow AV node conduction, ie digoxin, beta-blockers, adenosine or calcium channel blockers.
* The best choice is procainamide as it slows the accessory pathway. *If patient becomes hypotensive, cardiovert immediately!

38. Atrial Flutter

39. Atrial Flutter
Atrial activity of with sawtooth pattern. Usually a 2:1 conduction pattern; if it is 3:1 or higher, there is AV node damage
Treatment is to slow AV node conduction with amiodarone, propafenone or sotalol
DC cardiovert if <48 hours or unstable
You can also ablate the reentry pathway within the atrium between the tricuspid and the IVC.

40. Atrial Fibrillation

41. A-Fib
Can be due to HTN, cardiomyopathy, valvular heart desease, sick sinus, WPW, thyrotoxicosis or ETOH
Therapy is either rate control via slowing AV node conduction with stroke prophylaxis or rhythm control

42. Rate control Beta-blockers
Continuation after CABG may prevent a-fib
Good for hyperthyroid or post-MI patients with a-fib
 Carvedilol decreases mortality in patients with CHF
 Esmolol is good for acute management
 Digoxin actually increases vagal tone, thus indirectly slowing AV node conduction. But it is used essentially only in patients with LV dysfunction because it’s inotropic.

43. Rate control Calcium Channel Blockers
Nondihydropyridines (verapamil or dilitiazem) block AV node conduction but also have negative inotropy, so don’t use in CHF.
Dihydropyridines (nifedipine, amlodipine, felodipine) have no effect on AV node conduction
Adenosine is too short acting to be of any use in a-fib
Last choice is AV node ablation and permanent pacing

44. Rhythm control
Rhythm control does not decrease thromboembolic risk and may be proarrhythmic
Class 1A (quinidine, procainamide, disopyramide) slows conduction through HIS can cause torsades de pointes during conversion. They also enhance AV node conduction, so they should be used only after rate is controlled
Class 1B (lidocaine, meilitine, tocainide) are useless for a-fib
Class 1C (propafenone, and flecainide) slow conduction through HIS are good first choice.
Amiodarone is good if patient is post-MI or has systolic dysfunction.

45. Cardioversion for A-Fib
Cardiovert if symptomatic
Patients with a-fib for more than 2 days should be receive 3 weeks of anticoagulation before electrical cardioversion.
Give coumadin for 4 weeks after cardioversion

46. Anticoagulation Rules for A-Fib
Everybody who has rheumatic heart disease should be anticoagulated
If <65 yo and with h/o DM, HTN, CHF, CVA, prosthetic valves, thyrotoxicosis, LV dysfunction or LA enlargement, then give coumadin
If no risk factors, do nothing.
65-75 yo with any of above risk factors, give coumadin; if no additional risk factors, give coumadin or aspirin
>75 yo give coumadin but keep INR due to increased risk of bleed

47. Ventricular Tachycardia

48. Ventricular Tachycardia
Impulse is initiated from the ventricle itself
Wide QRS, Rate is
If unstable DC cardiovert
If not, IV Amiodarone and/or DCCV
Consider procainamide
Nonsustained ventricular tachycardia needs no treatment

49. Torsades de Pointes
“Twisting of the points” is usually caused by medication (quinidine, disopyramide, sotalol, TCA), hypokalemia or bradycardia especially after MI
Has prolonged QT interval
Acute: Remove offending medication. Shorten the QT interval with magnesium, lidocaine, isoproterenol, or temporary overdrive pacing
Chronic: may need pacemaker/ICD, amiodarone, beta-blockers

50. Ventricular Fibrillation
Most common in acute MI, also drug overdose, anesthesia, hypothermia & electric shock can precipitate
Absence of ventricular complexes
Usually terminal event
Use Amiodarone if refractory to DCCV.

51. Treatment
Here comes the fun part!

52. Classification of Anti-arrhythmics

53. Where did you say you worked?

54. When in doubt…Amiodarone

55. Amiodarone. Modes of action.
Mainly class III action on the outgoing K+ channels.
Class Ib action on the Na+ channels.
Non competitive alpha antagonism (class III)

56. Magnesium indications.
1. Torsades de point from any reason.
2. Arrhythmias in a patient with known hypomagnesaemia.
3. Consider its use in acute ischaemia to prevent early ventricular arrhythmias.
4. Digoxin induced arrhythmias.

57. Who gets a pacemaker?
 Syncope, presyncope or exercise intolerance that can be attributed to bradycardia
Symptomatic 2nd or 3rd degree AV block
Congenital 3rd degree AV block with wide QRS
Advanced AV block after cardiac surgery
Recurrent type 2 2nd degree AV block after MI
3rd degree AV block with wide QRS or BBB.

58. QUESTIONS