Basic ECG Interpretation tips for Allied Professionals

1. Essentials of ECG
Interpretation :
Pacemaker ECG, SVT &
VT

2. Electrocardiography
Electrocardiography (ECG) is a transthoracic interpretation of the
electrical activity of the heart over a period of time, as detected by
electrodes attached to the outer surface of the skin and recorded by
a device external to the body.[1]
"ECG- simplified. Aswini Kumar M.D". LifeHugger. Retrieved 2010-02-11.

3. Role of ECG
It helps in the detection of
Heart Attack & Coronary Artery Disease (Ischaemia)
Abnormal heartbeats (conduction system disorders)
Bradycardia
Tachycardia
Enlargement of cardiac chambers
Problems with the blood chemistry
Image source : http://potomachospital.blogspot.tw

4. Conduction System
Primary Pacemaker Rate / Min
SA Node 60-100
Escape Pacemaker
AV Node
AV Junction
HIS Bundle 40 - 60
Bundle Branches
Ventricles
Purkinje Fibres 20 - 40
Image source : http://www.ekgguru.com/content/conduction-system-illustration

5. Normal Sinus Rhythm
1:1 AV synchrony (one atrial event for each ventricular event)
Stable rhythm with repeating patterns (60 – 100 bpm)
Morphologies of beats should be similar from complex to complex
Rate should be appropriate—not too fast, not too slow
12 lead tracing source : http://meds.queensu.ca/courses/assets/modules/ts-ecg/Normal_ECG.bmp Video source : Youtube.com

6. ECG Complex

7. ECG Interpretation
• Step 1: What is the rate?
• Step 2: Is the rhythm regular or
irregular?
• Step 3: Is the P wave normal?
• Step 4: P-R Interval/relationship?
• Step 5: Normal QRS complex?
Image source : www.broward.edu/cehealth

8. Step 1 : Rate
Method 1 : Count the number of R waves for a six second interval
and multiply by ten.
6 sec
3 sec 3 sec
• Tachycardia exists if the rate is greater than 100 bpm.
• Bradycardia exists if the rate is less than 60 bpm.
3 1 1
Method 2 : 0 5 0 7 6 5
0 0 0 5 0 0

9. Step 2 - Rhythm
• Determine if the ventricular rhythm is regular or
irregular
• R-R intervals should measure the same
• P-P intervals should also measure the same
REGULAR
IRREGULAR

10. STEP 3 : P Wave
Morphology
• Identify and examine P waves:
• Present?
• Appearance?
• Consistency?
• Relation to QRS?

11. Standard Morphologies
Lea P- QRS T-
d Wave Wave
Limb Leads – Vertical Plane
I   
II   
III   
Augmented Leads
aVR   
aVF   
aVL   
Lea P-Wave QRS T-Wave
d
Precordial Leads – Horizontal Plane
V1 /± Small R wave / QS 
V2 /± Small R wave / QS 
V3  Equiphasic QRS / 
V4   
V5   

12. Step 4 : PR Interval
Consistent PRI of <.20 secs is normal
Lengthening of PRI is indicative of AV Nodal disease
Shortening of PRI is indicative of a bypass tract

13. Step 5 : QRS Duration
• A narrow QRS complex (< 0.12), indicates the
impulse has followed the normal conduction pathway
• A widened QRS complex (> 0.12), may indicate the
impulse was generated somewhere in the ventricles

14. Abnormal Cardiac Rhythm
• Abnormally shaped waves
• Lack of 1:1 AV synchrony
• Rapid cardiac activity, even if otherwise stable
• Very slow cardiac activity, even if otherwise stable
• Irregular cardiac activity
• Variability in PR interval
• Pauses
• Premature beats (oddly timed events)

16. Conduction Blocks

17. Function of a Pacemaker
• Sense intrinsic activity
• Pace the appropriate chamber

18. Systematic Approach
• Identify pacing mode
• Is there capture?
• Is there sensing?
• What is the pacing interval?
• Are there rate variations and can we account for them?
• Is hysteresis present?
• Is fusion or pseudofusion happening?

19. ECG # 1
• VVI.
• Capture is present.
• Sensing cannot be determined (this strip is all
pacing).
• The pacing interval corresponds to a rate of 72 ppm

20. Potential Problems Identifiable
on an ECG
• Undersensing
• Oversensing
• Noncapture
• No output
• Pseudomalfunction

21. Undersensing
• An intrinsic depolarization that is present, yet not
seen or sensed by the pacemaker
P-wave
not sensed
Atrial Undersensing
Common Causes of Undersensing
• Inappropriately programmed conductor fracture
sensitivity
• Lead maturation
• Lead dislodgment
• Change in the native signal
• Lead failure: Insulation break;

22. Oversensing
Markersensing of an
The channel shows inappropriate signal
...Though no
intrinsic activity... activity is present Ventricular Oversensing
Can be physiologic or nonphysiologic
Common Causes of Oversensing
• Lead failure sensitivity
• Poor connection at connector • Change in the native signal
block
• Exposure to interference
• Inappropriately programmed

23. Non – Capture
• No evidence of depolarization after pacing artifact
Loss of capture
Common Causes of Noncapture
• Lead dislodgment • Poor connection at
connector block
• Low output
• Lead failure
• Lead maturation

24. Functional Non-Capture
• Functional non-capture occurs when a pacing spike
is delivered at a time when it could not possibly
depolarize the heart (because the cardiac tissue is
refractory)
• However, had the pacing spike been more
appropriately timed, it might have captured the heart
• Functional non-capture is most often observed in
asynchronous (non-sensing) modes, such as VOO or
AOO

25. No Output
Pacemaker artifacts do not appear on the ECG; rate is
less than the lower rate
Pacing output delivered;
no evidence of pacing
spike is seen
Common Causes of No Output
• Poor connection at connector block • Battery depletion
• Lead failure • Circuit failure

26. Pseudomalfunction: Hysteresis
• Allows a lower rate between sensed events to occur;
paced rate is higher
Lower Rate 70 ppm Hysteresis Rate 50 ppm

27. Fusion
• Definition : The combination of an intrinsic beat and a paced beat
• The morphology varies, a fusion beat doesn't really look like a paced
beat or an intrinsic beat
• Fusion beats contribute to the contraction of the chamber being
paced
• VOO pacing @ 80 bpm, so there is no sensing going on.
• Capture is appropriate.
• Beats 7 and 8 are fusion

28. Pseudofusion
• The pacing pulse falls on an intrinsic beat
• The pacing pulse is ineffective and does not
contribute to the contraction of the chamber
• VVI, pacing @ 72 bpm
• Capture is present. Sensing is appropriate.
• Beats 3 and 6 are fused beats; beat 4 is an example of
pseudofusion.

29. Remember
• Identify pacing mode
• Is there capture?
• Is there sensing?
• What is the pacing interval?
• Are there rate variations and can we account for them?
• Is hysteresis present?
• Is fusion or pseudofusion happening?

31. Categorization of Tachycardia
using 12 Lead ECG
The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427–437

32. Mechanism of Arrhythmia
• Abnormal heart pulse formation
• Sinus pulse
• Ectopic pulse
• Triggered activity
• Abnormal heart pulse conduction
• Reentry
• Conduct block

33. SUPRAVENTRICULAR
TACHYCARDIA

34. Supraventricular
Tachycardia
• Arrhythmia originates ―above the ventricles‖
• Usually has a rapid Narrow QRS (ventricular) response
• Aberrant (abnormal appearing) conduction (SVTAC) can
produce a wide-complex tachycardia that may mimic
ventricular tachycardia (VT).
• To differentiate SVTs from true VTs
• If atrial rate>ventricular rate, the rhythm is likely to be an SVT
• If atrial rate=ventricular rate, the rhythm is likely to be a sinus
tachycardia or nodal reentry
• If the atrial rate<ventricular rate, the rhythm is likely to be a
VT

35. Common Forms of SVT
• SVTs from a sinoatrial source:
• Sinoatrial nodal reentrant tachycardia (SNRT)
• SVTs from an atrial source:
• Ectopic (unifocal) atrial tachycardia (EAT)
• Multifocal atrial tachycardia (MAT)
• Atrial fibrillation with a rapid ventricular response
• Atrial flutter with a rapid ventricular response
• Without rapid ventricular response, fibrillation and flutter are usually not classified as SVT
• SVTs from an atrioventricular source (junctional tachycardia):
• AV nodal reentrant tachycardia (AVNRT) or junctional reciprocating tachycardia (JRT)
• Permanent (or persistent) junctional reciprocating tachycardia (PJRT), a form of JRT which
occurs predominantly in infants and children but can occasionally occur in adults
• AV reciprocating tachycardia (AVRT) - visible or concealed (including WPW syndrome)
• Junctional ectopic tachycardia (JET)

36. Supraventricular
Tachycardia
Narrow complex, regular; retrograde P waves, rate <220

37. Differential Diagnosis for Narrow QRS
Tachycardia
Narrow QRS Tachycardia
(QRS < 120 ms)
Yes No
Regular Rhythm
No AF / AT / Flutter with
Visible P waves
variable AV conduction /
Yes MAT
No
Atrial Rate > Ventricular Rate
Yes
No
Atrial Flutter / AT Analyse RP Interval
Yes
Short (RP < PR) Long (RP > PR)
Yes
No
RP > 70
AT / PJRT / Atypical
RP < 70 ms
AVNRT
AVRT / AVNRT /
AVNRT
AT
ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias∗—executive summary. J Am Coll Cardiol.
2003;42(8):1493-1531. doi:10.1016/j.jacc.2003.08.013

38. AV Nodal Reentrant Tachycardia
Slow pathway
• 2 pathways within or
limited to perinodal
tissue
• Anterograde conduction
down fast pathway blocks
with conduction down slow
pathway, with retrograde
conduction up fast
pathway.
Fast pathway

39. ECG Pattern of Typical AVNRT
12-Lead ECG shows a regular SVT recorded at an ECG paper speed of 25
mm/sec. Note the pseudo r′ in V1 (arrow) and accentuated S waves in II, II, aVF
(arrow). These findings are pathognomonic for AVNRT.
ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias∗—executive summary. J Am Coll
Cardiol. 2003;42(8):1493-1531. doi:10.1016/j.jacc.2003.08.013

40. WPW Pathophysiology
• The atrial impulses are
conducted partly or
completely, prematurely,
to the ventricles via a
mechanism other than
the normal AV-node *
*Moss & Adams

41. Types of Accessory
Pathway
WPW - ORT
WPW – Manifest
AP
WPW – ART
Concealed AP URAP
Accessory
Pathway
PJRT
Mahaim

42. Algorithms

43. AVRT
• Antidromic atrioventricular reentrant tachycardia,
• Right posteroseptal accessory pathway.
• Note the wide-complex, regular rhythm. The delta waves are more prominent
because of maximal pre-excitation.
The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427–437

44. AVRT
• Orthodromic atrioventricular reentrant tachycardia.
• Note the narrow, regular, rapid tachycardia.
• The P waves buried in the ST segment (short-RP interval) are marked with an
arrow.
• No pseudo S/R’ waves are seen
The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427–437

45. Atrial Flutter
• P waves are present but have a
characteristic ―saw tooth‖ appearance
• Two types of flutter
• Type I is organized – i.e., saw tooth
appearance
• Type II is disorganized and appears as a
fib/flutter
• Best observed in leads II, III, and aVF.
Normal sinus rhythm
• Result of reentry within the atria
• Atrial rate is usually range between 220 -
Atrial Flutter
350

46. Atrial Flutter
• This atrial flutter shows distinctive atrial beats and the
characteristic sawtooth pattern
• Atrial rate here is 250 bpm
• Only every other atrial beat conducts down to the
ventricles, so the ventricular rate is 125 bpm
• P-waves are evident
• There are four p-waves to every ventricular beat (4:1
conduction)
• The atrial rate here is 280 bpm
• Atrial flutter with irregular ventricular response
• P-waves are evident; these are ―flutter‖ waves with
the characteristic flutter pattern
• Not every P-wave conducts but there is no regular
pattern; this indicates AV block

47. Atrial Fibrillation (AF)
• Disorganized, rapid atrial rhythm
• P-waves not clearly discernible
• Ventricular response is often rapid,
may be erratic
• Three main types of AF
• Paroxysmal
• Starts suddenly, resolves spontaneously,
short episodes, asymptomatic
• Persistent
• Longer duration, requires medical
intervention, likely symptomatic
• Permanent
• Chronic, medically refractory, often
severely symptomatic

48. Atrial Tachycardia
Ectopic foci within the atria, distinguished by a consistent p-wave of
abnormal morphology that fall before a narrow, regular QRS complex.
The 12-Lead Electrocardiogram in Supraventricular Tachycardia. Kumar et al. Cardiol Clin 24 (2006) 427–437

49. P-Wave Morphology in Focal
Atrial Tachycardia:
J Am Coll Cardiol. 2006;48(5):1010-1017. doi:10.1016/j.jacc.2006.03.058

50. Ventricular Tachycardia

51. Ventricular Tachycardia
(VT)
A VT is an abnormally fast rhythm that originates within
the ventricles, or more specifically in the region below
the His bundle.

52. Ventricular Tachycardia

53. Classification : Etiology
• Ischemic (Post MI) • Idiopathic VT
• Scar related – Not associated with any SHD –
unknown cause
• Slow conduction pathways
– Usually Focal mechanism
• Re-entry mechanism – Monomorphic
– RVOT (85%), RV inflow, RV inferior
wall
• LV ―outflow tract‖
• LCC, RCC, NCC
• coronary venous system
• LV idiopathic VT (verapamil sensitive)
• Basal LV
• Papillary muscles

54. Classification : Morphology & Duration
• Monomorphic VT - has one QRS shape or morphology
• Polymorphic VT - has more than one QRS shape.
• Nonsustained VT - short bursts of complexes lasting less than 30
seconds.
• Sustained VT- complexes lasting at least 30 seconds or that require
intervention in less than 30 seconds.

55. Distinguishing VT from SVT
Ventricular tachycardia (VT) is diagnosed by demonstrating that the atria are not part of the VT mechanism.
Since all VTs are potentially life-threatening, it is critical to distinguish VT from SVT with aberrant
conduction.
• AV dissociation is present in 50% of patients with VT. It is never present in SVT. During VT, retrograde
conduction over the AV node does not occur. Thus if AV dissociation occurs during extrastimulus pacing
but the tachycardia continues, the rhythm is almost always VT (Murgatroyd 2002).
• The table provides information for distinguishing VT from SVT with aberrancy.
More than 95% of patients with previous myocardial infarction and wide-complex QRS have VT regardless

56. QRS Complexes in different
types of WCT
Examples of leads V1 and V6 in
both left bundle branch block
and right bundle branch block
types of QRS complexes in
different types of wide complex
tachycardia. ECG,
electrocardiogram; SVT,
supraventricular tachycardia;
WPW, Wolff–Parkinson–White
syndrome.
Cara N. Pellegrini, Melvin M. Scheinman, Clinical Management of Ventricular Tachycardia, Current Problems in Cardiology, Volume 35, Issue 9,
September 2010

57. QRS Axis
The mean QRS axis is determined by the anatomic position
of the heart and the direction in which the activation wave
spreads through the ventricles.

58. Electrode Placements
4th intercostal space
Mason and Likar, Am Heart J 1966; Pahlm o, Am J Cardiol 1992; Pahlm O, J Eletrocardiol 2008

59. Lead Misplacement
QRS-T changes secondary to shift of the V4 electrode

60. Depolarisation
Tabatabaei and Asirvatham: Circ Arrhyth 2010

61. Lead Groups
• Inferior Leads
• II, III, aVF
• View from Left Leg
• Inferior wall of left ventricle
• Lateral Leads
• I, aVL, V5 and V6
• View from Left Arm
• Left lateral chest wall /
ventricle
• Anterior Leads
• V3, V4
• Left anterior chest
• electrode on anterior chest
• Septal Leads
• V1, V2
• Along sternal borders
• Look through right ventricle & see
septal wall

62. Predictors of VT

63. Predictors of VT
LBBB pattern
In V1 : QS in V6 : QR / QS / QrS / Rr’
Concordant pattern in precordials
Common in VT
-ve concordance in limb leads is another way of describing
NW axis and suggests VT

64. VT Localisation
The steps to finding the exit site are:
What is the bundle branch block (BBB)
configuration?
What is the inferior lead QRS complex
polarity?
What is the lead I QRS complex
polarity?
What is the lead aVL QRS complex
polarity?
What is the lead aVR QRS complex
polarity?
Where is the R-wave transition point?

65. Ventricular Tachycardia in the Absence of Structural Heart Disease. Srivathsan K, Lester SJ, Appleton CP, Scott
LR, Munger TM - Indian Pacing Electrophysiol J (2005)

66. Localization of VT
Using the twelve-lead electrocardiogram to localize the site of origin of ventricular tachycardia. Mark E. Josephson, MD,a David J.
Callans, MDb

67. Localization of VT
Using the twelve-lead electrocardiogram to localize the site of origin of ventricular tachycardia. Mark E. Josephson, MD,a David J.
Callans, MDb

68. Conclusion
• Always follow a systematic approach to reading ECGs
• Step 1: What is the rate?
• Step 2: Is the rhythm regular or irregular?
• Step 3: Is the P wave normal?
• Step 4: P-R Interval/relationship?
• Step 5: Normal QRS complex?
• Determine the site of origin of the arrhythmia
• Interpret the Waveform morphologies

69. A Warm Invitation….
…………to an Unforgettable
Experience !