ECG lecture for Internal Medicine Residents

1. ECG Interpretation
Upgraded
Done By : Abdullah Almazyad R2

2. What is an ECG ?
• It is a Graphical representation of Electarical Activity of the heart in a
specific time frame
• Mostly used to diagnose Heart Electricity Abnormality (Arrythmias) ,
however it can hint toward other Cardiac abnormality like Structural
heart disease (Hypertrophy)
• It can also hint to Non Cardiac conditions like PE (S1Q3T3) or ICP ,
even Electrolyte abnormality like hyperkalemia
• So there is great benefit can be extracted from an ECG

3. • 12 classical Leads :
• Chest Leads looks at the heart from Horizontal
Plane while the Limb Leads looks at the heart
From a Vertical plane
1-Bipolar Limb Leads : I / II / III :
Bipolar means that the lead mesures electarical potential
Between 2 of 3 limbs
2-Augmented Limb Leads : AvF / AvL / AvR :
Unipolar as they use one Limb electrode as a positive pole and
And take the average of input from the other two
3-6 Chest Leads : From V1-V6
You can ask for 15 Leads ECG for Posterior Wall MI

4. • https://www.youtube.com/watch?v=Rt4kjD4z8vM

5. What leads represent side of the heart ?
• Anterior Wall : V3-V4
• Septum : V1-V2
• Later Wall : Lead I , AvL , and V5-V6
• Inferior Wall : Lead 2 , 3 and AvF
• Posterior Wall : V7-V9
• Depolarization waves that goes toward a positive electrode give a positive
deflection
• Depolarization waves that goes from a positive electrode to a negative
electrode gives a negative deflection

7. Excitation Pathway

8. ECG Wave Representation

10. ECG Abnormality

12. • First thing first , make sure of name of pt and the date
• Always start by looking at the Calibiration (should be 2 large boxes) , so it
wouldn’t feel like you are zooming in or out giving you false representation
about size of each wave
• Also the speed should be 25mm/sec so it wouldn’t seems Tachycardiac or
Bradycardiac
• Then jump right into Checking if it is Sinus Rhythm or not , by looking and
appreaciating the P wave , should be present , upright in lead 2 , followed
by QRS then you should decide if Reguler or Irriguler

13. Next step is Rate

14. • Two ways to predict the rate either :
1-Devide 300 on the number of large boxes between a 2 QRS complex
(Used for Reguler Rhythm only)
2-the other way is to calculate how many QRS complexes in the whole
strip , then multiply that by 6 ( we say 6 because usually a whole strip
represent almost a 10 seconds , so if we multiply by 6 then this will give
us the rate in a minute) ------ Used for both Reguler and irriguler
rhythm

17. Next Step is Axis

19. • If Lead 1 and Avf both positive then this is normal Axis Deviation
• If Lead 1 is in negative deflection and AvF in a positive deflection
(Kissing Shape) then this is a Right Axis Deviation
• If Lead 1 is positive deflection and AvF in a negative Deflection (Away
from each other) then this is a Left Axis Deviation
• If both are on negative deflection then this is (No man’s Land)

20. • causes of right axis deviation
• normal finding in children and tall thin adults
• right ventricular hypertrophy
• chronic lung disease even without pulmonary hypertension
• anterolateral myocardial infarction
• left posterior hemiblock
• pulmonary embolus
• Wolff-Parkinson-White syndrome - left sided accessory pathway
• atrial septal defect
• ventricular septal defect
• causes of left axis deviation
• left anterior hemiblock
• Q waves of inferior myocardial infarction
• artificial cardiac pacing
• emphysema
• hyperkalaemia
• Wolff-Parkinson-White syndrome - right sided accessory pathway
• tricuspid atresia
• ostium primum ASD
• injection of contrast into left coronary artery

21. P Wave Abnormality
• Absent P Wave ?
• Too numerous ?
• Peaked ?
• Wide ?
• Multiple shapes ?

23. Atrial Fibrillation
• Absent P Waves
• Irriguler Rhythm
• Normal QRS Complex
• Ashman Phenomenon sometimes are present

25. Atrial Flutter
• Multiple P wave with some P waves Conducting to a QRS , sometimes
could be in a 2:1 appearance
• Atrial activity could reach up to 300
• Reguler Rhythm
• Loss of the isoelectric baseline
• Saw-Tooth Apearance

26. • Typical atrial flutter (Common, or Type I Atrial Flutter)
• Involves the IVC & tricuspid isthmus in the reentry circuit. Can be further
classified based on the direction of the reentry circuit (anticlockwise or
clockwise):
• Anticlockwise Reentry: Commonest form of atrial flutter (90% of cases).
Retrograde atrial conduction produces:
• Inverted flutter waves in leads II,III, aVF
• Positive flutter waves in V1 – may resemble upright P waves
• Clockwise Reentry: This uncommon variant produces the opposite pattern:
• Positive flutter waves in leads II, III, aVF
• Broad, inverted flutter waves in V1
• Atypical atrial flutter (Uncommon, or Type II Atrial Flutter)
• Does not fulfill criteria for typical atrial flutter
• Often associated with higher atrial rates and rhythm instability
• Less amenable to treatment with ablation

28. Multifocal Atrial Tachycardia
• Deffirent P Wave Morphology
• Irriguler Rhythm
• Dominant R Wave in V1
• Right Axis Deviation
Happens mostly due to Atrial Automaticity (the property of cardiac
cells to generate spontaneous action potentials which usually
happens due to Hypoxia)

30. P Pulmonale = RAE
• Right atrial enlargement produces a peaked P wave (P
pulmonale) with amplitude:
• > 2.5 mm in the inferior leads (II, III and AVF)
• > 1.5 mm in V1 and V2

32. P Mitral = LAE
• LAE produces a broad, bifid P wave in lead II (P mitrale) and
enlarges the terminal negative portion of the P wave in V1.
• In lead II
• Bifid P wave with > 40 ms between the two peaks
• Total P wave duration > 110 ms
• In V1
• Biphasic P wave with terminal negative portion > 40 ms duration
• Biphasic P wave with terminal negative portion > 1mm deep

34. P-R Interval Abnormality
• Short ?
• Depressed ?
• Prolonged ?

36. wolff parkinson white syndrome
• WPW syndrome is characterized by a double stimulation of the
ventricles. A premature conduction wave via accessory
pathways (pre-excitation) stimulates the portions of the
ventricles nearest the atrium; then the ventricles depolarize as a
result of the conduction wave which proceeds normally through
the atrioventricular (AV) node

37. • Short P-R Interval
• Narrow QRS Complex
• Delta Wave (Slurred QRS)

42. Heart Block
• First Degree Heart Block :
Prolonged PR Interval >200ms , each P wave is followed by QRS , No Drop , Bradycardia
• Second Degree Heart Block :
Mobits Type 1 :
Continues prolongation of PR Interval until a drop take place , Bradycardia
• PR interval is longest immediately before dropped beat
• PR interval is shortest immediately after dropped beat
Mobits Type 2 : Normal PR Interval , some P Waves are not followed by QRS Complex
Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node)
The risk of asystole is around 35% per year
Rhythm is Irriguler in these two
Third Degree Heart Block :
No relation between QRS Complex and P Waves , Rhythm is Reguler

45. • High Grade AV block
• Second degree heart block with a P:QRS ratio of 3:1 or
higher, producing an extremely slow ventricular rate
• For above example :
• High-grade AV block (4:1 conduction ratio).
• Atrial rate is approximately 140 bpm.
• Ventricular rate is approximately 35 bpm.
• Broad QRS complexes suggest that this may be due to Mobitz
II block

47. PeriCarditis
• Four Stages :
1.diffuse ST elevation with PR depression
2.resolution of stage 1 with TW flattening
3.deep symmetrical TW inversion
4.resolution

48. QRS Complex
• Wide ?
• Narrow ?
• Poor R-R Wave progression ?
• Low Voltage ?

50. SupraVentriculer Tachycardia
• AVNRT ? / AVRT ? / Atrial Tachy ?
In comparison to AVRT , which involves an anatomical re-entry
circuit (Bundle of Kent), in AVNRT (Most Common 65-75%) there
is a functional re-entry circuit within the AV node.

51. • With AVNRT usually the P Wave is buried within the QRS while in
AVRT the P wave is sometimes found in the ST Segment

52. Types of AVRT

54. SVT with aberrancy
• ECG features increasing the likelihood of VT :
• Absence of typical RBBB or LBBB morphology
• Extreme axis deviation (“northwest axis”): QRS positive in aVR and negative in I
and aVF
• Very broad complexes > 160ms
• AV dissociation:
• P and QRS complexes at different rates
• P waves are often superimposed on QRS complexes and may be difficult to
discern
• Capture beats: Occur when the sinoatrial node transiently “captures” the
ventricles in the midst of AV dissociation, producing a QRS complex of normal
duration
• Fusion beats: Occur when a sinus and ventricular beat coincide to produce a
hybrid complex

56. Wide QRS complex ?
• Ventriculer Tachycardia
• Ventriculer Fibrillation
• Vantriculer Pacing
• Right and Left Bundle Branch Block
• SVT with Abberancy

59. Ventriculer Tachycardia
• Could be Monomorphic VS Polymorphic
• Could be Sustained (>30 sec) VS NonSustained
• Criteria for diagnosis of VT using the 4-step Brugada algorithm:
• (i) Is RS complex present in any lead? -> if NO the rhythm is VT
(ii) Is the RS duration >100ms in any lead? -> if YES then the rhythm
is VT
(iii) Is there AV dissociation? (fusion or capture beats) -> if YES then
the rhythm is VT
(iv) Is the rhythm morphologically consistent with SVT (looks like
RBBB or LBBB)? -> if NO the rhythm is VT

62. Ventricular Febrillation
• Chaotic irregular deflections of varying amplitude
• No identifiable P waves, QRS complexes, or T waves
• Rate 150 to 500 per minute
• Amplitude decreases with duration (coarse VF –> fine VF)
• Le Syndrome de Haïssaguerre (idiopathic VF):
• Diagnosis of exclusion in patients who have survived a VF episode
without any identified structural or metabolic cause despite extensive
diagnostic testing

64. Ventricular Pacing

66. Premature Ventricular Contraction
• Broad QRS complex (≥ 120 ms) with abnormal morphology
• Premature , occurs earlier than would be expected for the next
sinus impulse
• Discordant ST segment and T wave changes.
• Usually followed by a full compensatory pause

67. Origin of Ectopic beats (PAC , PJC , PVC)
• Groups of pacemaker cells throughout the conducting system are
capable of spontaneous depolarisation
• The rate of depolarisation decreases from top to bottom: fastest at
the sinoatrial node; slowest within the ventricles
• Ectopic impulses from subsidiary pacemakers are normally
suppressed by more rapid impulses from above
• However, if an ectopic focus depolarises early enough — prior to the
arrival of the next sinus impulse — it may “capture” the ventricles,
producing a premature contraction
• Premature contractions (“ectopics”) are classified by their origin —
atrial (PACs), junctional (PJCs) or ventricular (PVCs)

68. • Unifocal — arising from a single ectopic focus; each PVC is
identical
• Multifocal — arising from two or more ectopic foci; multiple
QRS morphologie
• Bigeminy — every other beat is a PVC
• Trigeminy — every third beat is a PVC

70. Premature Atrial Contraction
• Abnormal (non-sinus) P wave usually followed by a normal
QRS complex (< 120 ms)
• Post-extrasystolic pauses may be present — PACs that reach
the SA node may depolarise it, causing the SA node to be
“reset”, with a longer-than-normal interval before the next sinus
beat arrives
• PACs may also be conducted aberrantly (usually RBBB
morphology), or not conducted at all. P waves will still be visible
in both cases

72. Premature Junctional Complex
• Beats origin is from AV Node
• Premature QRS complexes without a preceding P wave.
• The QRS morphology is very similar to the sinus complexes.

75. Right Bundle Branch Block
• QRS duration > 120ms
• RSR’ pattern in V1-3 (“M-shaped” QRS complex)
• Wide, slurred S wave in lateral leads (I, aVL, V5-6

76. • Sequence of conduction in RBBB:
1) Left ventricular activation via the left bundle (black arrow)
occurs normally
2) Septal depolarisation (yellow arrows) is thus unaffected,
producing a normal early QRS complex
3) Activation of the RV originates across the septum. The
resultant depolarisation vector (red arrow) produces delayed R
waves in leads V1-3, and S waves in lateral leads

77. Left Bundle Branch Block
• QRS duration > 120ms
• Dominant S wave in V1
• Broad monophasic R wave in lateral leads (I, aVL, V5-6)
• Absence of Q waves in lateral leads
• Prolonged R wave peak time > 60ms in leads V5-6

78. • Sequence of conduction in LBBB:
1) Conduction delay means impulses travel first via the right
bundle branch (black arrow)
2) Septum is activated from right-to-left (yellow arrows)
3) Overall depolarisation vector is directed towards lateral leads
(red arrow)

79. Smith-Modified Sgarbossa Criteria
• Concordant ST elevation ≥ 1 mm in ≥ 1 lead
• Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3
• Proportionally excessive discordant STE in ≥ 1 lead anywhere
with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the
preceding S-wave

80. Incomplete RBBB
• Incomplete RBBB is defined as an RSR’ pattern in V1-3 with
QRS duration < 120ms

81. Incomplete LBBB
• Incomplete LBBB is diagnosed when typical LBBB morphology
is associated with a QRS duration < 120ms.

82. • Left Anterior Fesciculer Block ?
• Left Posterior Fesciculer Block ?
• BiFesciculer Block ?
• TriFesciculer Block ?
Outside our scope , however we need to learn it as well

84. Low Voltage
• The amplitudes of all the QRS complexes in the limb leads are < 5
mm; or
• The amplitudes of all the QRS complexes in the precordial leads are
< 10 mm
Caused by :
-Pericardial effusion / Pleural effusion
-Obesity
-Constrictive Pericarditis
-Scleroderma

88. Right Ventricular Hypertrophy
• Right Axis Deviation of +110° or more.
• Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
• Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
• QRS duration < 120ms (changes not due to RBBB).

90. Poor R Wave Progression (PRWP)
• Poor R-wave progression (PRWP) is a common ECG finding
that is often inconclusively interpreted as suggestive, but not
diagnostic, of anterior myocardial infarction (AMI). PRWP is
defined by R wave height ≤ 3 mm in V3

91. ST Segament
• Depression ?
• Elevation ?

93. RV Strain
• ST depression and T wave inversion in leads corresponding to
the right ventricle:
• Right precordial leads V1-3 +/- V4
• Inferior leads II, III, aVF, often most pronounced in lead III as
this is the most rightward facing lead

97. • Anterior Wall : V3-V4
• Septum : V1-V2
• Later Wall : Lead I , AvL , and V5-V6
• Inferior Wall : Lead 2 , 3 and AvF
• Posterior Wall : V7-V9

99. Posterior Wall MI

101. De Wellens Syndrome
• Progressive symmetrical deep T Wave inversion in leads V2
and V3
• Slope of inverted T waves generally at 60°-90°
• Absence of ST Elevation
Indicate Critical Proximal Left Anterior Descending Artery Infarction
(LAD)

103. De Winter Phenomenon
• Tall, prominent, symmetrical T waves in the precordial leads
• Upsloping ST segment depression > 1mm at the J-point in the
precordial leads
• Absence of ST elevation in the precordial leads
• Reciprocal ST segment elevation (0.5mm – 1mm) in aVR
• “Normal” STEMI morphology may precede or follow the De
Winter pattern
It represent an anterior STEMI Equivalent

106. • This is a very worrying ECG demonstrating massive Anterolateral STEMI
with :
• Gross ST elevation in V1-6, I and aVL
• Early Q wave formation in aVL
• Reciprocal ST depression in inferior leads II, III and aVF
• This ECG pattern is seen in proximal LAD occlusion and indicates a large
territory infarction with a poor LV ejection fraction. These patients are at
high likelihood of Ventricular Fibrillation (VF), cardiogenic shock and
death, and require aggressive management both pre-hospital and in the
emergency department setting.
• Massive ST elevation often merges with hyperacute T waves in these
patterns creating the appearance of a broad QRS complex – this can be
mistaken for hyperkalemia or a broad complex tachycardia.

109. Pathological Q Wave
• Q waves are considered pathological if:
• > 40 ms (1 mm) wide
• > 2 mm deep
• > 25% of depth of QRS complex
• Seen in concurrent leads

110. T Wave
• HyperAcute ?
• Flattened ?
• Inverted ?

113. QT Interval
• Prolonged ?
• Shortened ?

116. • Hypocalcemia is associated with prolonged QT Interval
• HyperCalcemia is associated with Shotened QT Interval
• AntiPsychotic Meds ??
• For better assessment of QT Interval use equations provided in MD
Calc Like :
1-Bazett
2-Fridericia
3-Framingham

117. •Weird ECGs ??

121. Sick Sinus Syndrome
• Alternating bradycardia with paroxysmal tachycardia, often
supraventricular in origin.
• On cessation of tachyarrhythmia may be a period of delayed
sinus recovery called sinus pause or exit block.
• If significant this period of delayed recovery may result in
syncope.

128. Brugada Syndrome
• This ECG abnormality must be associated with one of the
following clinical criteria to make the diagnosis:
• Documented ventricular fibrillation (VF) or polymorphic
ventricular tachycardia (VT).
• Family history of sudden cardiac death at <45 years old .
• Coved-type ECGs in family members.
• Inducibility of VT with programmed electrical stimulation .
• Syncope.
• Nocturnal agonal respiration

129. • Type 1 :
Coved ST segment elevation >2mm in >1 of V1-V3 followed by a
negative T wave
• Type 2 :
has >2mm of saddleback shaped ST elevation
• Type 3 :
can be the morphology of either type 1 or type 2, but with <2mm of ST
segment elevation

131. Lead Misplacement
• This is limb electrode misplacement leading to Limb Lead
Reversal. A northwest axis in an ECG with normal precordial
leads simply does not make sense.
• Although we assume correct lead placement when interpreting
the ECG, an upright P-QRS-T complex in aVR with otherwise
normal QRS conduction should raise suspicion for limb lead
reversal.

132. How To Get Better ?
• Read ECGs daily using systematic approach
• Life in the Fast Lane
https://litfl.com/
• Dr.Alkhudhair weekly ECG Lectures in the CCU Conference Room

133. Thank you for your attendance and
participation