1. Heart Rate and Arrhythmia Basics
Kevin Formes D.O.
July 27, 2004

2. Cardiac Cycle Phase 0: Rapid depolarization
Sodium moves rapidly into the cell
Calcium moves slowly into the cell
Phase 1: Early repolarization
Sodium channels close
Phase 2: Plateau
Calcium continues to flow in
Potassium continues to flow out
Phase 3: Rapid repolarization
Calcium channels close
Potassium flows out rapidly
Active transport Na/k pump
Phase 4: Resting
Cell membrane is impermeable to sodium
Potassium moves out

3. Ventricular Action Potential & EKG
QRS T
0.2 sec

4. Heart Physiology: Sequence of Excitation
Figure 17.14a

5. Heart Physiology: Sequence of Excitation
Sinoatrial (SA) node generates impulses about 75 times/minute
Atrioventricular (AV) node delays the impulse approximately 0.1 second
Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

6. Electrocardiography
Electrical activity is recorded by electrocardiogram (EKG)
P wave corresponds to depolarization of atrium
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex

7. The 8-Step method Determine the rhythm Determine the rate
Determine the axis
Evaluate the p wave
Determine the duration PR interval
Determine the duration of QRS complex
Determine the duration of QT interval
Evaluate ST segment and T wave

8. Methods To Determine Rate
Distance between the R-R interval (300/#large blocks)
1 large block 300
2 large blocks 150
3 large blocks 100
4 large blocks 75
5 large blocks 60
6 large blocks 50

9. Lead Systems:
In 1902, Willem Einthoven recorded the first EKG. He determined that the heart lies at the center of the electrical field determined by the axis of three standard “Limb” electrodes.
Different “leads” or views of the electrical patterns produced were obtained by electrodes placed on the Left Arm, Right Arm, and Left Leg.

10. Electrocardiogram (EKG): Electrical Activity of the Heart
Einthoven's triangle
P-Wave – atria
QRS- wave – ventricles
T-wave – repolarization
Figure 14-20: Einthoven’s triangle

11. Cardiac Axis by different Leads
Carr and Brown Figure 8-2

12. Pathological Conditions Mean Electrical Axis (mark changes in current flow)
Left Axis Deviation (hypertrophy of left ventricle)
1. Hypertension (muscle mass on left side of heart)
2. Aortic Valvular stenosis
3. Aortic Valvular regurgitation
4. Several congenital heart conditions
Right Axis Deviation
1. Hypertrophy of right ventricle (pulmonary stenosis)
2. Tetralogy of Fallot (congenital right to left shunt )

13. Precordial (chest) Leads- V6 V5 V4 V3 V1 V2

14. Electrocardiogram (EKG): Electrical Activity of the Heart
≤100 msec
msec
≤ 450 msec

15. Normal Sinus Rhythm
Sinus node is the pacemaker, firing at a regular rate of bpm. Each beat is conducted normally through to the ventricles
One P wave for each QRS
PRI: seconds and constant
QRS: .04 to .1 seconds

16. Arrhythmias Bradycardia Tachycardia
1st degree AV block
2nd degree AV block
3rd degree AV block
Premature Ventricular Complex (PVC)
Atrial Fibrillation
Ventricular Tachycardia
Ventricular Fibrillation

17. Pathological Conditions That Lead to Arrhythmias
Ischemia
Intracellular Ca2+ overload
Stress: adrenergic stimulation
Genetic defects- especially in ion channels
Anatomic defects
Drug effects

18. Bradycardia: Rate less than 60
Disorders of impulse formation
Sinus bradycardia
Sinus node dysfunction (sick sinus syndrome
Junctional and ventricular escape rhythms
Disorders of impulse conduction (heart block)
1,2,3 degree AV block

19. Sinus Bradycardia Rate less than 60 Normal P waves, PR interval
Causes:
Overmedication
Inferior wall MI
Increased intracranial pressure
Hypothyroidism
Carotid Sinus hypersensitivity
Normal Variant
Treatment: Atropine, external or tranvenous pacing if symptomatic,
EP of no value diagnosis is derived from Clinical Hx, clinical judgement, and monitoring and correlation with symptoms

20. 1st Degree A-V Block Not really “block”
Just P-R interval longer than normal (> 0.2 sec)
Treatment: none

21. 2nd Degree AV Block Mobitz type 1
Some action potentials fail to get through the A-V node
Normal Sinus Rhythm
2nd degree A-V block
Treatment: none or ventricular pacing

22. 2nd Degree AV Block Type I
Progressive PR interval lengthening
Dropped QRS
AV nodal delay

23. 2nd Degree AV Block Type 2 Constant PR interval Dropped QRS
Infra-nodal delay- Treatment pacemaker

24. 3rd Degree A-V Block
No action potentials from the SA node/atria get through the A-V node
Normal Sinus Rhythm
3rd degree A-V block
Treatment: ventricular pacing

25. Junctional Rhythm
Originate from the area in and around the AV junction.
Inherent rate is 40-60
Enhanced automaticity may causes more rapid rates.
Electrical impulses are conducted backward (retrograde) to depolarize the atria and forward (antegrade) to the ventricles. Makes the p-wave inverted in lead II.

26. Where are those P waves?
Impulse from AV junction depolarizes atria before ventricles - p waves will be in front of QRS
Impulse from AV junction depolarizes ventricles before atria - p waves will be after QRS
Impulse from AV depolarizes atria and ventricles simultaneously - p wave will be hidden in the QRS

27. Tachycardia: Rate Greater Than 100 Causes
Increased automaticity:
atrial, junctional and ventricular premature complexes
Accelerated junctional rhythm
Accelerated idioventricular rhythm
Ectopic atrial rhythms
Some forms of VT
Triggered activity
Some forms of VT, long QT
Digoxin toxicity (Late after depolarizations)
Reentry
AV nodal reentrant tachycardia
AV reentrant tachycardia (WPW)
Atrial fibrillation
Atrial flutter
Most forms of VT

28. Delayed Afterdepolarization (DAD)
Occurs only after a “triggering” action potential
Intracellular Ca2+ overload
ischemia
digitalis intoxication
adrenergic stress
Na/Ca exchange generating depolarizing current
-50
200 msec
Action potential

29. Normal Action Potential Conduction
-50
200 msec
Action potential
Purkinje fibers
20 msec
Conduction times
(1 mm/msec):
A-C 10 msec
A-B 10 msec
C-B 10 msec A
10 mm
10 mm
10 mm B C
Ventricular Muscle

30. Re-entry Circuits as Ectopic Foci and Arrhythmia Generators
Atrio-Ventricular Nodal Re-entry
supraventricular tachycardia
Ventricular Re-entry
ventricular tachycardia
Atrial Re-entry
atrial tachycardia
atrial fibrillation
atrial flutter
Atrio-Ventricular Re-entry
Wolf Parkinson White
supraventricular tachycardia

31. Differential Diagnosis of Tachyarrhythmias
Narrow complex:
Regular-sinus tachycardia, ectopic atrial tachycardia, atrial flutter, junctional tachycardia, AVNRT, AVRT
Irregular- Atrial fibrillation, multifocal atrial tachycardia, atrial flutter with variable conduction
Wide complex
Regular- Ventricular tachycardia, supraventricular tachycardia with aberrancy
Irregular-Atrial fibrillation with aberrancy

32. Sinus Tachycardia
Sinus node is the pacemaker, firing regularly at a rate of greater than 100 times per minute. Each impulse is conducted normally through to the ventricles
Almost always occur as a response to some physiological stimulus (fever, exercise, volume depletion, thyrotoxicosis, hypotension
If symptomatic use AV nodal blocking agents (CCB,BB, Dig)

33. Atrial Flutter Reentrant circuit around tricuspid valve
Flutter waves at (avg 300/min)
AV conduction ratio 4:1, 3:1 ect
“Saw-toothed” waves
Treatment with ablation works around 99% of the time

34. Atrial Fibrillation Irregular irregularity R-R interval variablity
Rate greater than
Two types-bad atrial tissue secondary to HTN, ischemia or bad pulmonary vein tissue young patients

35. Causes of Atrial Fibrillation
Pulmonary disease
Ischemia
Rheumatic heart disease
Anemia, atrial myxoma
Thyroid
Electrolytes
Sepsis

36. Atrial Fibrillation Treatment
Try to restore normal rhythm (cardioversion) only within 48 hrs
vagatonic maneuvers (carotid massage, Valsalva maneuver, gagging)
adenosine
If persistent rhythm:
control ventricular rate (calcium channel blocker, beta blocker)
anticoagulant therapy (coumadin)

37. Multifocal Atrial Tachycardia
Multiple P wave morphology
Multiple PR intervals
Irregular irregularity
Associated with COPD, hypoxia, and theophylline toxicity
Treat underlying cause, or AV node ablation with pacemaker

38. AV Nodal Reentrant Tachycardia
Results from a small micro-reentrant circuit within the AV node itself
Is usually initiated by a premature atrial beat
EKG tachycardia with no p waves or p waves after the QRS complex
Treatment is AV nodal-blocking drugs (CCB,BB,Dig)

39. Atrioventricular Reentrant Tachycardia
Involves a large reentrant loop with one limb of the circuit including the AV node and the other being an abnormal connection between the atria and ventricles (WPW)
Usually initiated by PVC
Two types-
Orthodromic (narrow complex QRS) 90%, Antidromic (wide complex QRS) 10%
IF AV nodal blocking agents are given with a-fib and avrt could cause V-fib

40. Ventricular Tachycardia
Usually associated with symptoms
Rate: (200±50); at least 3 ectopic QRS in row
QRS: normally wide and bizarre
Usually associated with MI or other organic HD; unusual in normals
Often serious requiring quick treatment if sustained
Mechanism? Reentry or rapid firing ectopic??
Treatment: cardioversion, lidocaine

41. Ventricular Fibrillation
Multiple foci in the ventricles become irritable and generate uncoordinated, chaotic impulses that cause the heart to fibrillate rather than contract.
Treatment: cardioversion

42. Asystole
The heart has lost its electrical activity. There is no electrical pacemaker to initiate electrical flow.
Treatment: ACLS protocol, transcutaneous pacing, epinephrine 1mg IVP q3 to 5, atropine 1mg q 3 to 5

43. Premature Atrial Contraction
Early beat that originates in the atria as an ectopic pacemaker
Etiology
Usually caused by enhanced automaticity in atrial tissue
May be a single or multiple ectopic sites
Shape of the p-wave depends on the location of the ectopic beat

44. Premature Atrial Contraction
P-wave configuration
Usually different from the underlying p-wave
QRS configuration
Usually similar to the underlying rhythm
If very early, the bundle branches may not have repolarized sufficiently for normal conduction. (usually conducted left and blocked right)

45. Non-compensatory pause
* measurement between the R-wave preceding the PAC to the R-wave following the PAC is less than two R-R cycles of the underlying rhythm

46. Compensatory Pause
* measurement between the R-wave preceding the PAC to the R-wave following the PAC equals two R-R cycles of the underlying rhythm

47. Antiarrhythmic Drugs
Class I: Local anesthetic action, reducing Na channel current
Lidocaine, Quinidine
Class II: b-Adrenergic antagonists
Propranalol
Class III: action potential prolongation
Amiodarone
Class IV - Ca channel antagonists
Verapamil

48. Quiz
Name the Rhythm # 1:

49. Answer:
Atrial Flutter

50. Name the Rhythm #2:

51. Sinus Bradycardia

52. Name the Rhythm #3:

53. Third Degree Heart Block

54. Name the rhythm # 4:

55. Ventricular Fibrillation

56. Name the rhythm #5:

57. Normal Sinus

58. Name the rhythm #6:

59. AV Block 2 Degree (type 1)

60. Name the rhythm # 7:

61. Atrial Fibrillation

62. Name the rhythm # 8:

63. Ventricular Tachycardia

64. Name the rhythm # 11:

65. Sinus Tachycardia