1. Cardiac Arrhythmias
An Introduction:
Dr.S.Nandakumar.

2. Starting with the Basics …
What are the functions of the heart?
Electrical: “impulse”
Mechanical: “pump” “contraction”
What is the normal electrical pathway conduction?
Nodes (SA, AV, Bundle)
Inherent Rates

5. Electrical Conduction Pathway
SA Node – “pacemaker” of
the heart (60-100bpm)
AV Node – junction of the
atria and ventricles (40-60bpm)
Bundles – Bundle of His
connects the AV node to the
bundle branches (20-40bpm)

6. Normal Cardiac Cycle Systole Diastole Electrical Depolarization
“activate”
Repolarization
“recovery”
Mechanical
Contract
“empty”
Relax
“fill”

7. Depolarization and Repolarization
Current spread through 3 components
Pace maker cells
conduction pathways
Heart muscle itself

8. feeds the right atrium and ventricle
Blood supply
Right Coronary Artery
feeds the right atrium and ventricle
inferior wall
posterior wall
SA Node and AV Node (in most people)
Left Anterior Descending
anterior wall and intraventricular septum
bundle branches
Circumflex
lateral and posterior wall of L Ventricle

9. ECG What does it tell us? Electrical conduction through the heart
Areas of ischemia or myocardial infarction
LV Hypertrophy
Electrolyte disturbances / drug toxicity

10. Components of ECG

11. ECG Tracing ………. Grid Paper Each small box = 0.04 seconds
One large box = 0.20 seconds
5 large boxes = One second
30 large boxes = Six seconds
300 large boxes = 1 minute

12. What Is In Each Beat?
P Wave – atrial contraction or depolarization, (usually upright)
QRS Complex – ventricular depolarization (usually upright) ( sec) (delays in the bundle branches will widen the QRS)
T Wave – ventricular repolarization “recharging” (usually upright)
PR Interval – time between atrial depolarization to ventricular depolarization ( sec) (prolonged PR ..
QT Interval – represents one complete ventricular depolarization and repolarization (beginning of QRS to the end of the T wave) (0.32 – 0.44sec) (disturbances are usually due to electrolyte disturbances or drug effects)

13. Reading a Rhythm Strip
Rate - Is the rate normal (60-100), slow, or fast?
Regularity - What is the R – R Interval?
P Wave – Is there a P wave before every QRS? Is it upright?
QRS Complex – Is it normal following each P wave? Wide or normal?
T wave – How does your T wave look? Upright?
Measure your intervals – PR Interval, QRS, QT

14. “Practice Strip”

16. Lt.Atrial Hypertrophy

19. What is an Arrhythmia ?
Definition: An abnormal electrical conduction that changes the heart rate and rhythm.
*Some are mild, asymptomatic – require no treatment

20. Why are we so concerned with Arrhythmias?
What is The Big Deal?
Why are we so concerned with Arrhythmias?
SV x HR = Cardiac output
Stroke Volume dependent on filling time, and
myocardial muscle function
HR dependent on electrical stimulus, Autonomic NS
Too Fast
Too Slow NOT GOOD!!!
Too Irregular

21. “Clinical Significance”
Dysrhythmias are responsible for over 44,000 deaths each year.
About 15% of strokes occur with atrial arrythmias
A large majority of sudden cardiac deaths are due to ventricular dysrhythmias.

22. The causes of the cardiac arrhythmias
1. Abnormal rhythmicity of the pace maker.
2. Shift of the SA node to another place & spontaneous generation of impulses.
3. May be Blocks in the spread of the impulse.
4. Abnormal pathways.

23. Mechanisms of arrhythmogenesis
Increased automaticity
Triggered activity
Re-entry

24. Abnormal automaticity
The sinus node contains pacemaker cells that have spontaneous firing capacity. This is called normal automaticity.
Abnormal automaticity occurs when other cells start firing spontaneously, resulting in premature heartbeats. All cardiac cells have spontaneous firing capacity.
During a normal heart rate, they never have the chance to show off their firing capacity. But during extreme bradycardia, other cells can take over the function.

25. Increased automaticity
Examples:
Catecholamines
Electrolyte imbalance
Ischemia
Hypoxia
Drugs

28. Triggered activity
During triggered activity heart cells contract twice, although they only have been activated once.
This is often caused by so called afterdepolarizations (early or delayed afterdepolarizations EADs / DADs) caused by electrical instability of the myocardial cell membrane.

29. Triggered Activity Afterdepolarisations Examples: Digitalis
Accelerated ventricular Rhythm following reperfusion in MI

30. Re-entry circuits and ectopics –basis of arrhythmias.

31. The mechanism of re-entry
Re-entry can occur when there are two alternative pathways with different conducting properties (e.g. an area of normal tissue and an area of ischemic tissue).
In this example, pathway A conducts slowly while pathway B conducts rapidly
(1) In sinus rhythm each impulse may pass down both pathways (normal & ischemic) and then enter common distal pathway.
(2) Since the pathways A & B recover at different rates and so when pathway B may recover, a premature impulse that comes through pathway A, may travel up retrograde to pathway B, setting up a closed loop or re-entry circuit.
(3) This may initiate a tachycardia that will continue until the circuit is interrupted by a electrical depolarization

32. Re-entry circuits and ectopics –basis of arrhythmias.

34. Classification of arrythmias
1. Characteristics:
a. tachycardia – increased rate
c. bradycardia – decreased rate
b flutter – very rapid but regular
contractions
d. fibrillation – disorganized
contractile activity

35. Classification of arrhythmias
Narrow complex tachyarrhythmias
Broad complex tachyarrhythmias
Bradyarrhythmias

36. Narrow complex tachyarrhythmias
Sinus tachycardia
SA nodal reentrant tachycardia
Paroxysmal atrial tachycardia
Multi-focal atrial tachycardia
AVNRT
AVRT
Atrial Flutter
Atrial Fibrillation

37. Broad complex tachyarrhythmias
SVTs with aberrancy
Accelerated Idioventricular rhythm VT VF

38. Bradyarrhythmias Sinus bradycardia Sinus node dysfunction
AV conduction disturbances

39. Sinus node dysfunction
Sick sinus syndrome
Bradycardia-tachycardia syndrome

40. AV conduction disturbances
First degree AV block
Second degree AV block
Type 1 (Wenkebach’s phenomenon)
Type 2
Complete heart block

41. First degree AV block
Prolonged PR interval

42. Type 1 Second degree AV Block (Wenkebach’s Phenomenon)
Gradual beat by beat prolongation of PR-interval and then resulting in a dropped beat

43. Type 2 Second degree AV Block
Fixed PR interval, but intermittent dropped beats
Beats may be dropped irregularly or follow a regular pattern (Eg. 2:1, 3:2)

44. Complete Heart Block
Atrial depolarisations are completely prevented from reaching the ventricles at the AV node
Slow Idioventricular rhythm occur
AV dissociation

46. Atrial Fibrillation No P Wave!
Repetitive, irregular, uncontrolled depolarization. Atrial rate ~ bpm
No P Wave!
No PR Interval
Loss of “Atrial Kick”
Emboli Potential

48. COMMON CAUSES OF ATRIAL FIBRILLATION
Coronary artery disease (including acute myocardial infarction)
Valvular heart disease, especially rheumatic mitral valve disease
Hypertension
Sinoatrial disease
Hyperthyroidism
Alcohol
Cardiomyopathy
Congenital heart disease
Chest infection
Pulmonary embolism
Pericardial disease
Idiopathic (lone AF)

49. Arrhythmias stemming from the ventricles
Arrhythmias stemming from the ventricles. Occurs when a pacemaker in the ventricles initiate a beat
Premature Ventricular Contraction (PVC)
QRS wide and bizarre
Ventricular Tachycardia (V Tac)
3 or more ventricular ectopic complexes lead to V tac.
Rate greater than bpm
QRS complex wide and aberrant

52. 3 or More PVCs = Ventricular Tachycardia

53. Ventricular tachycardia
Ventricular tachycardia: a broad complex tachycardia
Sustained V. Tach. Is usually a life-threatening arrhythmia, that can degenerate into ventricular fibrillation

54. Ventricular tachycardia
Physical Exam:
If patient is relatively stable, “cannon a waves” can appear in the neck (AV dissociation)

55. Sustained V- Tac

56. Ventricular Fibrillation (V Fib)
The ventricle depolarizes at a rapid uncontrolled manner
No recognizable waves and complexes
V Fib is the most lethal arrhythmia and will be fatal!

59. Torsades de pointes
–literally twisting of the points. (Triggered activity)
This form of polymorphic ventricular tachycardia is a complication of prolonged ventricular repolarisation (prolonged QT interval).

60. Bundle Branch Block Interruption of conduction
in one of the main branches
of the Bundle of His
QRS wide – greater than 0.12 seconds

63. Pharmacologic Considerations
Above the AV NODE (Atrial) (ABCD)
Too Slow Atropine
Too Fast Beta Blockers
Calcium Channel Blockers Digoxin
Amiodarone
Below the AV NODE (Ventricular) (LAP)
Too Fast Lidocaine
Amiodarone Procainamide

64. And you feel all rhythms look alike, look Closely and you will see the differences!

65. Thank You