1. Cardiac Arrhythmias II: Tachyarrhythmias
Michael H. Lehmann, M.D.
Clinical Professor of Internal Medicine
Director, Electrocardiography Laboratory

2. Supraventricular Tachycardias
(Supraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region)

3. Supraventricular Tachycardia (SVT) Terminology
QRS typically narrow (in absence of bundle branch block); thus, also termed narrow QRS tachycardia
Usually paroxysmal, i.e, starting and stopping abruptly; in which case, called PSVT
“Paroxysmal Atrial Tachycardia (PAT)” - the older term for PSVT - is misleading and should be abandoned

4. AV Junctional Reentrant Tachycardias
(typically incorporate AV nodal tissue)

5. Mechanism of Reentry Bidirectional Unidirectional Recovery of
Conduction
Unidirectional
Block
Recovery of
Excitability
& Reentry

6. AV Nodal Reentrant Tachycardia

7. AV Nodal Reentrant Tachycardia Circuit
F = fast AV
nodal pathway
S = slow AV
nodal pathway
(His
Bundle)
During sinus rhythm, impulses
conduct preferentially
via the fast pathway

8. Initiation of AV Nodal Reentrant Tachycardia
PAC
PAC
PAC = premature atrial
complex (beat)

9. AV Nodal Reentrant Tachycardia
Sustainment of
AV Nodal Reentrant Tachycardia
Rate
beats per min
P waves
generated
retrogradely
(AV node
 atria) and
fall within or
at tail of QRS

10. Sustained AV Nodal Reentrant TachycardiaP P P P
Note fixed, short RP interval mimicking r’ deflection of QRS

11. Orthodromic AV Reentrant Tachycardia
Anterogade
conduction
via normal
pathway AP
Retrograde
conduction
via accessory
pathway (AP)

12. AV ReentrantTachycardia
Initiation of Orthodromic
AV ReentrantTachycardia
PAC
Atria AP
AVN
Ventricles
PAC = premature atrial
complex (beat)

13. AV Reciprocating Tachycardia
Sustainment of Orthodromic
AV Reciprocating Tachycardia
Atria
Rate
beats per min AP
AVN
Ventricles
Retrograde P’s fall
in the ST segment
with fixed, short RP

14. Ventricular Preexcitation (Wolff-Parkinson-White Syndrome)
Accessory Pathway with
Ventricular Preexcitation
(Wolff-Parkinson-White Syndrome)
Sinus
beat
Hybrid
QRS shape
“Delta” Wave
PR < .12 s AP
Fusion activation
of the ventricles
QRS  .12 s

15. Ventricular Preexcitation
Varying Degrees of
Ventricular Preexcitation

17. Intermittent Accessory Pathway Conduction
V Preex
V Preex
Normal
Conduction
Note “all-or-none” nature of AP conduction

18. Orthodromic AV Reentrant Tachycardia
NSR with
V Preex
Note
retrograde
P waves
in the
ST segment
SVT:
V Preex
gone

19. Concealed Accessory Pathway
Sinus
beat
No Delta wave
during NSR
(but AP capable
of retrograde
conduction)

20. Summary of AV Junctional Reentrant Tachycardias
Reentrant circuit incorporates AV nodal tissue
P waves generated retrogradely over a fast pathway
Short, fixed RP interval

21. Clinical Significance of AV Junctional Reentrant Tachycardias
Rarely life-threatening
However, may produce serious symptoms (dizziness or syncope [fainting])
Can be very disruptive to quality of life
Involvement of an accessory pathway can carry extra risks

22. Atrial Tachyarrhythmias

23. Sinus Tachycardia (100 to 180+ beats/min)
P waves oriented normally
PR usually shorter than at rest

24. Causes of Sinus Tachycardia
Hypovolemia ( blood loss, dehydration)
Fever
Respiratory distress
Heart failure
Hyperthyroidism
Certain drugs (e.g., bronchodilators)
Physiologic states (exercise, excitement, etc)

25. Premature Atrial Complex (PAC)V5
Non-Compensatory
Pause P P P P’ P
Timing of
Expected P

26. Premature Atrial Complex (PAC): Alternative Terminology
Premature atrial contraction
Atrial extrasystole
Atrial premature beat
Atrial ectopic beat
Atrial premature depolarization

27. PACs: Bigeminal Pattern
Note deformation of T wave by the PAC
“Regularly Irregular” Rhythm

28. PACs with Conduction Delay/Block
Physiologic
AV Block P P’
Physiologic
AV Delay P P’
Recovered
AV Conduction P P’

29. (Physiologic Delay in the His Purkinje System)
PAC with “Aberrant Conduction”
(Physiologic Delay in the His Purkinje System) V1 P P P’ P
RBBB

30. PACs with Aberrant Conduction (Physiologic RBBB and LBBB)V1
RBBB
LBBB
Normal
conduction

31. PACs with Physiologic LBBB and His-Purkinje System BlockV1
Non-conducted
PAC

32. Non-Conducted PAC V5 V1 P P P’ P
Note deformation of T wave by the PAC

33. Bigeminal/Blocked PACs Mimicking Sinus BradycardiaV1
Only the 4th
bigeminal PAC
conducts

34. Clinical Significance PAC’s
Common in the general population
May be associated with heart disease
Can be a precursor to atrial tachyarrhythmias

35. Atrial Tachycardia V1 RP intervals can be variable Differs from
RP often > PR
(Example slower than more common rate mof beats per min)
Differs from
AV nodal or
AV reentrant
SVT

36. Clinical Significance of Atrial Tachycardia
Similar to sequela of AV junctional reentrant tachycardias
Must be differentiated from them diagnostically

37. (“Typical,” Counterclockwise)
Atrial Flutter
(“Typical,” Counterclockwise)
Reentrant
mechanism

38. Atrial Flutter Classic inverted II “sawtooth” flutter waves
at 300 min-1
(best seen in
II, III and AVF) II
4:1
2:1 V1
Note variable
ventricular
response

39. Atrial Flutter V. rate 2:1 140-160 Conduction beats/min (common)
2:1 & 3:2
Conduction
1:1
Conduction
(rare but
dangerous)

40. Atrial Fibrillation Focal firing or multiple wavelets Chaotic, rapid
atrial rate at
beats per min

41. Atrial Fibrillation V5 V1 Rapid, undulating baseline (best seen in V1)
Most impulses block in AV node  Erratic conduction

42. Atrial Fibrillation: Characteristic
“Irregularly Irregular” Ventricular Response II

43. Rapid Ventricular Response
Atrial Fibrillation with
Rapid Ventricular Response II
Irregularity may be subtle

44. of Ventricular Response
Atrial Fibrillation: Autonomic Modulation
of Ventricular Response
Baseline
Immediately after exercise

45. Clinical Significance of Atrial Flutter and Fibrillation
Causes
Usually occur in setting of heart disease; but sometimes see “lone “ atrial fibrillation
Hyperthyroidism (atrial fibrillation)
May acutely precipitate myocardial ischemia or heart failure
Chronic uncontolled rates may induce cardiomyopathy and heart failure
Both can predispose to thromboembolic stroke, etc

46. Ventricular Preexcitation
Varying Degrees of
Ventricular Preexcitation

47. Atrial Fibrillation with
Rapid Conduction Via Accessory Pathway

48. Atrial Fibrillation with Third Degree AV Block
Regular ventricular rate reflects dissociated
slow junctional escape rhythm

49. Regular Narrow QRS Tachycardias

50. Differential Diagnosis of Regular Narrow QRS (Supraventricular) Tachycardia
Reentrant SVT incorporating AV nodal tissue
AV nodal reentrant tachycardia
Orthodromic AV reentrant tachycardia
SVT mechanism confined to the atria
Sinus tachycardia
Atrial flutter
Other regular atrial tachycardias
Short-RP favors AV node-dependent reentrant SVT

51. Determining AV Nodal Participation in SVT by Transiently Depressing AV Nodal Conduction
Vagotonic Maneuvers
Carotid sinus massage
Valsalva maneuver (bearing down)
Facial ice pack (“diving reflex;” for kids)
Adenosine (6-12 mg I.V.)
If SVT “breaks,” a reentrant mechanism involving the AV node is likely
If atrial rate unchanged, but ventricular rate slows (#P’s > #QRS’s), SVT is atrial in origin

52. SVT Responses to AV Nodal Depressant Maneuvers
SVT termination
AV nodal reentrant tachycardia
Orthodromic AV reentrant tachycardia
No SVT termination (despite maximal attempts)
Sinus tachycardia
Atrial flutter or fibrillation
Most atrial tachycardias (a minority are “adenosine-sensitive”)

53. Carotid Sinus Massage Stimulation of carotid sinus triggers
baroreceptor
reflex and
increased vagal
tone, affecting
SA and AV
nodes

54. Vagotonic Maneuver (Carotid Sinus Massage)
Termination of SVT by
Vagotonic Maneuver (Carotid Sinus Massage)

55. SVT
Carotid Sinus Massage

56. SVT
Adenosine 6 mg P P P P

57. Ventricular Tachyarrhythmias

58. Premature Ventricular Complex (PVC): Alternative Terminology
Premature ventricular contraction
Ventricular extrasystole
Ventricular premature beat
Ventricular ectopic beat
Ventricular premature depolarization

59. Premature Ventricular Complex (PVC)
Compensatory
Pause

61. PVCs: Bigeminal Pattern
“Regularly Irregular” Rhythm

62. Accelerated Idioventricular Rhythm
( Ventricular Escape Rate, but  100 bpm)
Fusion
beat
Ectopic
ventricular activation
Sinus
acceleration
Normal
ventricular activation

63. AV Dissociation ATRIA AND VENTRICLES ACT INDEPENDENTLY SA Node
Ventricular
Focus

64. Ventricular Tachycardia (VT)
Rates range from beats/min
Non-sustained or sustained
P waves often dissociated (as seen here)

65. Ladder Diagram of AV Dissociation During Ventricular Tachycardia
Slower atrial rate
Faster ventricular rate
Impulses invade the AV node retrogradely and anterogradely,
creating physiologic “interference” and block. Under the right
conditions, some anterograde impulses may slip through.
This phenomenon is not equivalent to third degree AV block

66. Ladder Diagram of AV Dissociation During Third Degree AV Block
Faster atrial rate
Slower ventricular (escape) rhythm
Note that impulses block anterogradely and retrogradely
within the AV conduction system

67. Monomorphic VT

68. Polymorphic VT V1

69. Causes of PVC’s and VT
PVC’s are fairly common in normals but are also seen in the setting of heart disease
Monomorphic VT often implies heart disease, but can sometimes be seen in structurally “normal” hearts
Polymorphic VT can result from myoardial ischemia or conditions that prolong ventricular repolarization
Electrolyte derangements, hypoxemia and drug toxicity can cause PVC’s and VT

70. MI Scar-Related Sustained Monomorphic VT Circuit

71. (Polymorphic VT Associated with Prolonged Repolarization)
“Torsade de Pointes”
(Polymorphic VT Associated with Prolonged Repolarization)

72. Clinical Significance of PVC’s and VT
Can be a tip-off to underlying cardiac, respiratory or metabolic disorder
VT may (but need not invariably) lead to hemodynamic collapse or more life-threatening ventricular tachyarrhythmias, increasing the risk of cardiac arrest

73. Ventricular Flutter VT  250 beats/min, without clear isoelectric line
Note “sine wave”-like appearance

74. Ventricular Fibrillation (VF)
Totally chaotic rapid ventricular rhythm
Often precipitated by VT
Fatal unless promptly terminated (DC shock)

75. Sustained VT: Degeneration to VF

76. Atrial Fibrillation with Rapid Conduction
Via Accessory Pathway: Degeneration to VF

77. Diagnosing Regular
Wide QRS Tachycardia

78. VT or SVT with Aberrant Conduction?
Regular Wide QRS Tachycardia:
VT or SVT with Aberrant Conduction? V1

79. Sustained Aberrant ConductionV1

80. Clinical Clues to Basis for Regular Wide QRS Tachycardia
REMEMBER: VT does not invariably cause hemodynamic collapse; patients may be conscious and stable
History of heart disease, especially prior myocardial infarction, suggests VT
Occurrence in a young patient with no known heart disease suggests SVT
12-lead EKG (if patient stable) should be obtained

81. VT or SVT with Aberrant Conduction?
Regular Wide QRS Tachycardia:
VT or SVT with Aberrant Conduction?

82. More R-Waves Than P-Waves Implies VT!II

83. Artifact Mimicking “Ventricular Tachycardia”
QRS complexes “march through”
the pseudo-tachyarrhythmia
Artifact
precedes
“VT”