1. Cardiac arrhythmias can be caused by disorders of impulse formation, disorders of impulse conduction, or a combination of the two. Disorders of impulse formation include abnormalities in automaticity and triggered activity. 2. Abnormal automaticity occurs when an ectopic pacemaker fires at an inappropriate rate, taking over control of the heart rhythm from the normal sinus node. Triggered activity is initiated by afterdepolarizations following an action potential. 3. Disorders of impulse conduction include conduction block and reentry, which is when an impulse circles back and reactivates tissue that is still recovering, leading to sustained, rapid rhythms. Common reentrant arrhythmias include atrial flutter, at

1. Mechanism of Arrhythmias
Dr Fuad Farooq

2. Normal Sinus Rhythm
Implies normal sequence of conduction, originating in the sinus node and
proceeding to the ventricles via the AV node and His-Purkinje system
EKG Characteristics:
Regular narrow-complex rhythm
Rate 60-100 bpm
Each QRS complex is proceeded by a P wave
P wave is upright in lead II & downgoing in lead aVR

3. The mechanisms responsible for
arrhythmias are generally divided into
–
–
–
Disorders of impulse formation
Disorders of impulse conduction
Combinations of both
cardiac

4. Disorders of Impulse Formation
Can be
– Disorder in Automaticity
– Trigger activity

5. Automaticity
Automaticity is the property of a fiber to initiate an
impulse spontaneously, without need for prior stimulation
Characterized by
– Inappropriate discharge rate of the normal pacemaker, the
SA node (e.g., sinus rates too fast or too slow for the
physiologic needs of the patient)
– Discharge of an ectopic pacemaker that controls atrial or
ventricular rhythm
Ectopic pacemakers are often called latent or subsidiary
pacemakers

6. Automaticity
Ectopic pacemakers are usually suppressed by
overdrive suppression by the more rapidly firing SA node
or by concealed conduction from neighboring fibers
– Manifested when the SA discharge rate slows or block
occurs at some level between the SA node and the ectopic
pacemaker site
– The discharge rate of the latent pacemaker can speed
inappropriately and usurp control of cardiac rhythm from
the SA node

7. Recognizing Altered Automaticity on EKG
Gradual onset (warming) and termination of the
arrhythmia
The P wave of the first beat of the arrhythmia is
typically the same as the remaining beats of the
arrhythmia (if a P wave is present at all)

8. Decreased Automaticity
Sinus Bradycardia

9. Increased/Abnormal Automaticity
Sinus tachycardia
Ectopic atrial tachycardia
www.uptodate.com
Junctional tachycardia

10. Triggered Activity
•
Triggered activity is initiated by after-depolarizations, which
are depolarizing oscillations in membrane voltage induced by
one or more preceding action potentials
•
Thus, triggered activity is pacemaker activity that results
consequent to a preceding impulse or series of impulses,
without which electrical quiescence will occurs

11. Phase 1: Initial
rapid
repolarization
Phase 0 : Rapid
depolarization
•Closure of the
fast Na+ channels
•Phase 0 and 1
together
correspond to
the R and S
waves of the
ECG
•Opening of fast Na
channels
Phase 4: Resting
phase
•Associated with
diastole portion of
heart cycle
•Potassium outward
current through
open, inwardly
rectifying K+ channels
( Ikl )
Phase 2 Plateau
phase
Phase 3 Repolarization
•K+ channels remain open
•Allow K+ to build up outside the cell,
causing the cell to repolarize
•Corresponds to T wave on the ECG
•Balance between
the inward
movement of Ca+ and
outward movement
of K +
•Corresponds to ST
segment of the ECG

12. Can be:
• Early after-depolarizations (EADs), arise from a reduced level of
membrane potential during phases 2 (type 1 – augmented
opening of Ca channels) and 3 (type 2 – augmented opening of
Na channels) of the cardiac action potential
• Late or delayed after-depolarizations (DADs), occur after
completion of repolarization (phase 4 – secondary to increase
cytosolic Ca++ levels), generally at a more negative membrane
potential than that from which EADs arise

14. • Causes of EAD include:
1. Low potassium blood level
2. Slow heart rate
3. Drug toxicity (i.e. quinidine causing torsades de
pointes)
• DAD may cause triggered activity due to:
1. Premature beats
2. Increased serum Ca++ level
3. Increased adrenaline levels
4. Digitalis toxicity

15. Disorder of Impulse Conduction
Can be:
– Conduction block
– Re-entry

16. Mechanism of Reentry

17. Mechanism of Reentry

18. Reentrent Rhythms
AV nodal reentrant tachycardia (AVNRT)
AV reentrant tachycardia (AVRT)
– Orthodromic
– Antidromic
Atrial flutter
Atrial fibrillation
Ventricular tachycardia

19. Recognizing Reentry on EKG
Abrupt onset and termination of the arrhythmia
The P wave of the first beat of the arrhythmia is
different as the remaining beats of the
arrhythmia (if a P wave is present at all)

20. Example of AVNRT

21. Atrial Flutter
Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the
right atrium

22. Atrial Fibrillation
Atrial fibrillation is caused by numerous wavelets of depolarization spreading
throughout the atria simultaneously, leading to an absence of coordinated
atrial contraction

23. Thank You