Systematic ECG Interpretation

1. ECG Interpretation
Dr S. A. Medway
SCGH EDCMEThursday 12/03/2015
Original Presentation Credit to Dr. James Wheeler

2. Resources
• Original Presentation – Dr JamesWheeler
• Erics Medical Lectures –YouTube
• LITFL
• emin5.com
• Time on the floor

3. What is an ECG?
• Graphical representation of the electrical activity of the myocardium over
time
• Standard 12 lead ECG assesses this in various planes (coronal & transverse)
to give a roughly 3D view of the heart
– 3 biploar leads I, II, III
– 9 unipolar leads aVR, aVL, aVF,V1-V6
– Can consider other unipolar lead placements
– V1-6R – look at RV
– V7-9 – look at post LV wall

4. Lead placement

5. Anatomical relationship

6. ANATOMICAL RELATIONSHIP OF LEADS

7. Considerations
• Methodical systematic approach
– “More is missed by not looking than by not
knowing"[Thomas McCrae, 1870-1935]
• Consider patients clinical condition
• Obtain previous ECG’s for comparison
• Limitations of ECG – Electrical activity, not
contractility etc…
• The “ normal” ECG
– All normal ECG’s do not look the same
– But they do have features in common

8. ECG helps in detection of:
– Ischaemic heart disease, acute or chronic
– Dysrrhythmias
– Electrolyte disturbances
– Conduction abnormalities (HB, BBB)
– CAD (exercise stress test)
– Cardiac structural abN (LVH, RVH)
– Cardiac manifestations of non-cardiac disease
(PE, metabolic disorders, lung disease…)

9. COMPONENTS OF ECG
• Rate
• Rhythm / Regularity
• Cardiac Axis
• Waveform (axis, amp, duration)
– P wave
– QRS complex
– T wave
– U wave
• Intervals
– PR interval
– QT interval
– RR interval
• Segments
– PR segment
– ST segment

10. ECG systematic evaluation
• Calibration / Speed
– N = 10mm/1mV, 25mm/sec
• Rhythm
– Regularity / QRS width / Rate
• Axis
– N / LAD / RAD
• P wave
– ?presence / relationship to QRS
– Axis
– Amp: RAA / LAA
• PR interval
– Duration / HB / Pre-excitation
• PR segment
– Depression
• QRS
– duration / amplitude / morphology
– Q waves
– R wave
• ST segment
– Depression / elevation / morphology
• T wave
– Axis / morphology / duration
• QT interval
• U wave
• Other waves (delta, osborne, epsilon, pacing
spikes, artifacts)
• ?other leads (V4R,V7-9, Lewis)

12. Normal ECG

13. ECG Rhythm
• Rate
– N / tachy / brady
• Regularity
– Regular / reg irreg / irreg irreg
• QRS morphology
– Narrow / wide (120ms)
• P waves
– Absent
– Present / morphology / relationship QRS / PR interval

14. ECG Rhythm
• Is it normal sinus rhythm (NSR)?
– Can you identify P waves
– P waves preceding all the QRS complexes
– QRS complexes after every P wave
– Normal PR interval
– Regular
• P waves most easily seen in II &V1
• If not – it’s not Sinus Rhythm. What is it??

15. Arrhythmias - Causes
• Abnormal impulse generation
– SA node
– Outside of the SA node
• Abnormal impulse conduction
– Damaged conduction pathways
– Re-entrant pathways

16. Note: there are many potential pacemaker sites in the heart!

21. AXIS (Coronal Plane)
• Axis of any ECG depolarisation or repolarisation
• QRS axis in the coronal (frontal) plane as determined
by the limb leads :
– bipolar (I, II, III) &
– unipolar (aVR, aVL, aVF)
• Normal axis determined largely by the relative size of
both the RV & LV, and the position of the heart
– may change in various pathological conditions

22. Determining QRS axis
• Normal QRS coronal axis
is (??) -30 to +90
degrees:
Both I & aVF +ve = normal
Both I & aVF -ve = EAD
lead I -ve & aVF +ve = RAD
lead I +ve & aVF -ve
lead II +ve = normal
lead II -ve = LAD
N
RAD
LAD
EAD

23. Normal ECG

24. Right axis deviation

25. Causes of RAD
• RVH (most common)
• Acute RH strain - Pulmonary embolus
• Dextrocardia
• Normal in children and tall thin adults
• Chronic lung disease even without pulmonary hypertension
• Left posterior hemiblock
• Lateral / apical AMI
• WPW syndrome - left sided accessory pathway
• Atrial septal defect
• Ventricular septal defect

26. Left axis deviation

27. Causes of LAD
• ?LVH
• Left anterior hemiblock
• LBBB
• Q waves of inferior myocardial infarction
• Artificial cardiac pacing
• Emphysema
• WPW syndrome - right sided accessory pathway
• Tricuspid atresia
• Ostium primum ASD

28. Causes of extreme axis deviation
• Emphysema
• Hyperkalaemia
• Lead transposition
• Artificial cardiac pacing
• Ventricular tachycardia

29. Transverse axis of QRS / Rotation
• Normal transverse axis is leftward and posterior:
– Hence usually a progression in R wave height fromV1 to
V6
• Transitional lead (where R = S)
– usuallyV3 orV4
• Displacement of transition:
– Right (V1,V2) = counterclockwise rotation
– Left (V5,V6) = clockwise rotation

30. Normal ECG

31. WAVE MORPHOLOGY
• Shape
• Axis
• Duration
• Amplitude
• Progression

32. P wave - Normal
• Normal P wave
– Represents atrial depolarisation
– Axis 0 – 75 deg
– Upright monophasic I, II, III and AVF
– Inverted in AVR
– Biphasic inV1 (RA bf LA)
– <2.5mm (0.25mV) in height limb leads
– <1.5mm in praecordial leads
– <3mm (120ms sec) in width
Lead II

33. Normal ECG

34. P wave - Abnormalities
• Morphology
• RAH (Pulm HTN) increased amplitude
• LAH (MS, HTN) notched in I & II, deep -ve inV1
• A Fib/Flut no clear P waves / sawtooth
• Hyperkalaemia reduced amplitude
• Ectopic atrial rhythm
• Axis
• Retrograde
• Dextrocardia right displacement
• Pulmonary disease inferior displacement
• Congenital heart disease left displacement
• Rhythm
• Ectopic atrial rhythm
• A Fib / flutter
• Multifocal atrial tachycardia
• SVT (retrograde P waves)

35. P wave – RAE / LAE

37. PR Interval - Normal
• Start of the P wave - start of the QRS
• Normal = 120 – 200ms
= 3 - 5 small squares
• Increases with age
• Is rate dependent
• Delay at AV node
» Protect ventricles
» Allow for ventricular filling

38. PR interval - Abnormal
• Short
– Preexcitation of ventricles (WPW) & other SVT’s
– AV junctional rhythm
– Exercise induced tachycardia
• Long
– AV Block
– Hyperkalaemia
– CHD
– Drugs (Digoxin, B-Blockers, Quinidine)
– Hypothermia
– Hypothyroidism

40. PR segment
• Normally isoelectric using theTP (not ST) segment as a
baseline
• Abnormal:
– Elevation
• Myocarditis (aVR,V1)
• Atrial infarction
– Depression
• Myo/pericarditis
• Atrial infarction
• Exercise induced tachycardia

42. QRS parameters
• Q waves
– ?abnormal Q’s
• R wave
– Progression
– Dominant R wave in aVR /V1
• QRS amplitude
• QRS duration (<100ms)

43. QRS waveform nomenclature
R r qR qRs Qrs QS
Qr Rs rS qs rSr’ rSR’

44. QRS complex – Q waves
• Normal Q waves
– Due to rightward septal depolarisation
– May occur in I, II,III, aVR, aVF, aVL,V4-V6
– Size <0.4mV (4 squares) or 25% of R wave height
– Duration <0.03sec (under 1 square)
– May be slightly greater in III & aVR (normal variant)
– No Q waves inV1-V3
• Abnormal Q waves
– >0.4mV (4 squares) or 25% of R wave height
– >0.03sec (ie. 1 square or greater)
– Presence inV1-3
– Suggest: evolved AMI / ventricular enlargement / rotation of heart /
HOCM / abnormal conduction / lead misplacement

45. Normal ECG

47. QRS – R wave Abnormalities
• Dominant R waveV1
– normal in children / young adults / persistent juvenile pattern
– RVH / PE / L to R shunt
– RBBB
– Post AMI (= Q wave)
– WPW type A
– Dextrocardia
– HOCM
– Muscular dystrophy
– Incorrect lead placement
• Dominant R wave aVR (>3mm, or R/S ratio >0.7)
– Na channel blockade
– Dextrocardia
– RVH
– Incorrect lead placement
• Poor R wave progression
– Prior anteroseptal AMI / LVH / incorrect lead placement / dextrocardia / normal variant

51. QRS abnormal amplitude:
• Increased
• LVH (S inV1 + R inV5 orV6 >35mm sensitive but not specific)
• BER
• Hyperthyroidism
• Normal / athletes
• Decreased (<5mm limb leads, <10mm precordial)
• Pericardial / Pleural effusion
• Hypothyroidism
• Pneumothorax
• Restrictive cardiomyopathy
• COPD
• Haemochromatosis
• Fluctuating / Electrical alternans

54. QRS prolonged duration:
• Causes
– BBB (may be rate related)
– Ventricular origin /Ventricular pacing
– Hyperkalaemia
– Na channel blockade
– Pre-excitation
– Hypothermia

56. ST Segment - Normal
• Represents period between depolarisation & repolarisation
(J point toT wave)
• Normally isoelectric with respect toTP & PR segment
• Abnormal if:
– Elevated
– Depressed

57. Normal ECG

58. ST segment - Elevation
• Morphology
– Concave - some non-AMI causes
– Convex - suggestive of AMI
• Distribution
– Widespread - ?non-AMI
– Localised to anatomically contiguous leads - suggestive of AMI
• Magnitude
– Larger suggestive of AMI
• QRS morphology
– Large amplitude - consider LVH
– Widening - consider BBB or vent. paced rhythm

59. ST segment elevation causes:
• AcuteCoronary Syndrome
• Acute pericarditis
• Benign early repolarisation (BER)
• LV aneurysm
• LVH
• BBB
• Left - R to mid precordial leads
• Right - lateral leads
• Cardiomyopathy
• Acute myocarditis
• Hypothermia
• Hyperkalaemia
• Myocardial contusion
• CNS injury
• Brugarda Syn
• Paced vent. Rhythms
• Post-electrical cardioversion

61. BER
- Prominent, assymetrical, concordant (with QRS)T waves
-Widespread concave ST segmentsV2-5
- J point elevation (notching / slurring)
- <25%T wave height inV6 (usually <2mm precordial)
- No reciprocal ST depression
- Stable over time

64. ST Segment - Depression
• Morphology
– Flat or downsloping with ACS
• Distribution
• QRS morphology
– Large amplitude - consider LVH
– Wide complex - BBB, vent. Pacing, LVH

65. ST segment depression causes:
• ACS (>1mm depression at J point, diffuse, horizontal or downsloping, not
localising)
• AMI (NSTEMI, Post MI, reciprocal)
• BBB
• LVH
• Ventricular pacing
• Digoxin effect
• Rate related
• Myocardial contusion
• Metabolic
• Post-electrical cardioversion

68. T wave - Normal
• Magnitude
– No clearly defined range (<5mm limb, <15mm precordial)
– General rule - 1/2 the height of preceding QRS
• Axis
– Largely dependent onQRS (concordant)
– Positive in I, II,V3-V6
– Negative in aVR,V1
– Variable in III, aVF, aVL, &V2

69. Normal ECG

70. T wave - Abnormalities
• Prominent
• AMI (hyperacute), Hyperkalaemia, BER, Myopericarditis (concave STE & PR
depression), BBB (esp. LBBB inV1-V3), LVH (similar to LBBB)
• Inverted
• ACS (all stages) NB may be flattened
• Wellen’s Syn. (critical prox LAD stenosis without MI) NB may be biphasic
• Past MI
• Pericarditis
• Children / Persisting juvenile pattern (V1-V3)
• CNS injury/ICH
• BBB
• PE, RVH, LVH, HOCM, Digoxin, toxic, metabolic

77. U wave
• Positive deflection that occasionally occurs afterT wave
• Most visible at slow HR’s inV1-V4
• The origin is uncertain (repol of the IVS)
• Presence or absence does not signify pathology
• Abnormal if:
– >1/3 precedingT wave height (N 1-2mm)
– Disconcordant withT wave

78. U wave - Abnormalities
• Increased amplitude
• Athletes
• Bradycardia
• HypoK+ / HypoCa2+ / HypoMg2+
• CNS event
• Hypertension
• Hypothermia
• Medications (digoxin, quinidine)
• Inversion
• Ischaemia
• LV overload
• RV overload
• PE

81. QT interval - Normal
• Measured from the start of the QRS to the
end of theT wave
– Measure in II,V 5-6
– use slope
– include U waves if continuous withT wave
• Represents the time required for ventricular
activation & recovery
• Range 330 - 440ms (460ms women)
• Rule of thumb < half RR interval
• QT interval corrected to the heart rate

82. QTc calculation
• Multiple formulas
• Bazett’s
– QTc = measured QT interval
 R-R interval
• Hence QTc = QT at HR of 60bpm

83. QTc - Abnormal Duration
• Short
– Hypercalcaemia / Digoxin / Congenital
• Long
– lengthened repolarisation time
– ventricle more susceptible to early after depolarisation which can precipitate a variety of potentially fatal arrhythmias (VF, VT, torsades de
pointes)
– Congenital long QT syndromes
– CNS disease
– Metabolic syndromes (HYPO: K+, Ca++,T4)
– Hypothermia
– Drugs:
• erythromycin, cisapride, amiodarone, haloperidol, quinidine…

86. Overview
• Rate & rhythm
• Axis
• Wave morphology
• Intervals
• Segments
• In the context of:
– Look at the patient (hear the story)
– Compare to old ECG’s
– Get a second opinion