Electrocardiogram Basics, Recognition of common pathologies and treatment of common ECG abnormalities

1. ECG BASICS
Dr Nirmal Shanmugam
Junior Resident
Department of Anesthesiology, Pain Medicine,
Critical Care
AIIMS New Delhi
*LOL. Buckle up!

2. Picture of an early ECG recording performed by Willem Einthoven in 1903

3. What is an ECG?
◦ A plot of voltage on the vertical axis v/s time on the
horizontal axis.
◦ It is a galvanometer that records potential difference.
◦ The Needle is deflected a given distance depending on
the voltage measured.
◦ Pattern recognition is important but it is important to
review all of its aspects to not miss anything.

4. ECG GRID

6. ECG LEADS AND DIRECTIONS

7. 60-100 bpm
60bpm
40-60bpm
30-40bpm
30-40bpm
10-30bpm

8. COMPLEXES AND INTERVALS

9. P wave :
◦ Atrial Depolarization
◦ Mostly positive ; Biphasic in V1 – Right atrial depolarization is directed
anteriorly while left atrial depolarization is directed posteriorly
◦ Duration: <0.12 sec (3 small boxes)
◦ Amplitude: <0.25 mv (2.5 small boxes)
◦ Atrial T wave is hidden in QRS complex
◦ During tachycardia, the Atrial T wave get unmasked causing J point depression
and appear like ST depression

10. PR Interval (from beginning of P wave to start of QRS)
◦ Atrial depolarization (the P wave) and conduction through the AV node and the His-
Purkinje system
◦ Length of the PR interval changes with heart rate - normally 0.12 to 0.20 sec (3-5 small
boxes)
◦ Shorter at faster heart rates - sympathetically mediated enhancement of atrioventricular
(AV) nodal conduction and vice versa

11. QRS complex
◦ Ventricular depolarization
◦ Initial negative deflection is called Q wave – normal in leads I, aVL and V4-V6 due to
septal depolarization
◦ The first positive deflection is called R wave - represents left ventricular depolarization.
◦ S wave - negative deflection following the R wave - terminal depolarization of the high
lateral wall.
◦ Duration - 0.06 to 0.10 seconds (1½ to 2½ small boxes) - not influenced by heart rate
◦ R wave should progress in size across the precordial leads V1-V6
◦ Lower case letters (q, r, or s) - relatively small amplitude waves of less than 0.5 mV

12. ST segment
◦ Ventricular depolarization has ended and before repolarization has begun.
◦ Electrocardiographic silence (Isoelectric line)
◦ J point - intersection of the end of the QRS complex and the initial part of the ST
segment
T wave
◦ Ventricular repolarization
◦ Broad, has a slow upstroke, and a more rapid downslope to the isoelectric line following its
peak.
◦ Usually smooth up and down ; Irregularity - a superimposed P wave should be considered.

13. QT interval
◦ Consists of the QRS complex, the ST segment, and T wave
◦ Primarily a measure of ventricular repolarization - JT interval - more accurate measure of ventricular
repolarization ; but clinically QT interval is used.
◦ QT (or JT) interval is dependent upon the heart rate
◦ Bazett’s formula :
QTc = QT interval ÷ square root of the RR interval (both measured in seconds)
◦ Problems : Inaccurate at heart rate extremes ; Units are erroneous – denominator is expressed as a
unitless quantity
◦ Other logarithmic regression formulas and algorithms have been proposed.
◦ Upper normal value : Men - ≤440 ms ; Women - ≤450 to 460 ms
◦ QRS widens in the setting of a bundle branch block – Modified formulas

14. U wave
◦ Precordial leads V2 to V4
◦ Due to late repolarization of the mid-myocardial M cells - longer action
potential duration compared with the endocardium or epicardium
◦ Amplitude - less than 0.2 mV
◦ More evident in bradycardia and hypokalaemia
◦ May merge with T wave and cause the QT-U wave – Digoxin and Hypercalcemia

15. APPROACH TO ECG
INTERPRETATION

16. Step 1: Rate
◦ If the cardiac rhythm is regular,
Rate = 300/Number of large boxes between R-R
OR
Rate = 1500/Number of small boxes between R-R
◦ Alternatively, Rate = 60/Time between subsequent QRS complexes(sec)
◦ If the rhythm is irregular – count the number of complexes for 10 seconds on the ECG and
multiplying by 6.
◦ In adults, rate of 60-100 beats per minute is normal.
◦ A rate less than 60 beats/min is bradycardia
◦ A rate over 100 beats/min is tachycardia

17. Step 2: Rhythm
Step 1: Locate the P wave
◦ Are P waves visible? – Maybe located within the T wave. Absence may indicate atrial fibrillation.
◦ What is the rate of the P waves (i.e., the PP interval)?
◦ What is the morphology and axis of the P waves?
Step 2: Establish the relationship between P waves and the QRS complex
◦ Are the P waves associated with QRS complexes in a 1:1 fashion?
◦ What is the PR interval like?
◦ Do P waves occur after each QRS complex?

18. Step 3: Analyze the QRS morphology
◦ If the QRS complexes are of normal duration (<0.12 sec) and morphology - rhythm is supraventricular
◦ QRS is wide (i.e., >0.12 sec) - rhythm is supraventricular with aberrant conduction
Step 4: Search for other clues
◦ Breaks in the rhythm or other irregularities in an otherwise regular rhythm
◦ Do the QRS complexes occur at regular intervals or are they irregular?
◦ Is rhythm regularly irregular (i.e., there is a repeating pattern of irregularity)
◦ Is the rhythm irregularly irregular
Step 5: Interpret the rhythm in the clinical setting

19. Step 3: Axis
◦ Normal QRS electrical axis (established in the frontal plane) : -30⁰ to
90º
◦ Left axis deviation : -30º to -90º
◦ Right axis deviation : 90º to 180º
◦ Extreme right or left axis: -90º and -180º
◦ QRS axis moves leftward during growth from 30 to 190º at birth to 0 to 120º
during ages 8 to 16 years
Method 1 : Axis can be determined by looking at leads I, II, aVF
Method 2 : Find the most isoelectric lead (Biphasic QRS complex) – the
axis would be perpendicular to this lead
Method 3 : Find the maximum positive deflection on the frontal lead –
axis would be parallel to this lead

21. Right Axis Deviation
◦ Normal variation (vertical heart with an axis of
90º)
◦ Mechanical shifts, such as inspiration and
emphysema
◦ Right ventricular hypertrophy
◦ Right bundle branch block
◦ Left posterior fascicular block
◦ Dextrocardia
◦ Ventricular ectopic rhythms
◦ Pre-excitation syndrome (Wolff-Parkinson-White)
◦ Lateral wall myocardial infarction
◦ Secundum atrial septal defect
Left Axis deviation
◦ Normal variation (physiologic, often with age)
◦ Mechanical shifts, such as expiration, high
diaphragm (pregnancy, ascites, abdominal tumour)
◦ Left ventricular hypertrophy
◦ Left bundle branch block
◦ Left anterior fascicular block
◦ Congenital heart disease (primum atrial septal
defect, endocardial cushion defect)
◦ Emphysema
◦ Hyperkalaemia
◦ Ventricular ectopic rhythms
◦ Pre-excitation syndromes (Wolff-Parkinson-White)
◦ Inferior wall myocardial infarction.

22. AXIS IN THE HORIZONTAL AXIS
◦ Imagining the heart as viewed from under
the diaphragm.
◦ If the axis is rotated in the clockwise
direction – LV forces are directed posteriorly
– Poor R wave progression
◦ If there is a counterclockwise rotation – LV
forces are directed anteriorly – tall R wave in
V2

23. ECG INTERPRETATION (CONTD.)
◦ Step 4: Intervals – PR; QRS; QT
◦ Step 5: P wave – Shape and axis ; rhythm; amplitude and duration
◦ Step 6: QRS complex – Morphology ; Voltage
◦ Step 7: ST segment-T wave – Elevation or depression relative to TP segment;
inversion of T waves
◦ Step 8: Overall interpretation

24. ABNORMALITIES

25. WHAT CAN AN ECG DIAGNOSE?
◦ Arrhythmias
◦ Myocardial Ischemia and Infarction
◦ Pericarditis
◦ Chamber hypertrophy
◦ Electrolyte disturbances
◦ Drug Toxicity (Digoxin and other drugs prolonging QT interval)

26. ARRHYTHMIAS

27. ASYSTOLE
◦ Rhythm will nearly be a flatline
◦ No rate ; P, QRS or T waves
◦ Start CPR

28. MANAGEMENT
◦ Check the patient's rhythm, taking less than 10 seconds to assess
◦ Verify the presence of asystole in at least two leads
◦ Resume High Quality CPR at a compression rate from 100-120 per minute.
◦ As soon as IV or IO access is available, administer epinephrine 1mg IV/IO q 3-5min
◦ Rule out and treat possible contributing causes ("Reversible Causes", H's and T’s)
◦ Check rhythm
◦ If no electrical activity is present (patient is in asystole), resume CPR.
◦ If electrical activity is present, see if the patient has a pulse.
◦ If the patient does not have a pulse or there is some doubt about the pulse, resume CPR.
◦ If a good pulse is present and the rhythm is organized, begin post-resuscitative care.
◦ IV/IO access is a priority over advanced airway management - advanced airway is placed, change to continuous chest
compressions without pauses for breaths. Give 10 breaths per minute (once every 6 seconds) and check rhythm every 2
minutes.
◦ Without a pulse or electrical activity on the ECG, the emergency care team needs to decide when resuscitation efforts
should stop. The patient's wishes and the family's concerns need to be considered

29. Approach to Bradyarrhythmia

30. SINUS BRADYCARDIA
◦ RR and PP intervals are regular
◦ Rate < 60 beats per minute
◦ PR and QRS duration normal
◦ Causes – SAN abnormalities, Hyperkalemia, Hypothermia, Hypothyroidism, Hypoxia, Increased ICP, CCBs or Beta
blockers, OSA, Vagal stimulation
◦ Treat symptomatic bradycardia

31. MANAGEMENT
◦ Rapidly ensure the stability of the patient's condition
◦ Continuous cardiac monitoring and intravenous access
◦ Stable patients – attempt to find the cause of the bradycardia
◦ If Secondary to drugs like Beta blockers, CCBs or Digitalis – discontinuation of the drug is
enough
◦ Hypothermia - Rewarming and supportive measures are the mainstays of therapy. (Atropine and
pacing may cause myocardial irritability)
◦ Pacing and Atropine Boluses are used in symptomatic patients

32. Assess appropriateness of clinical
condition; Heart rate <50/min
Identify and treat the underlying cause:
• Maintain patent airway
• Oxygen
• IV access
• 12 lead ECG (only if available)
Persistent bradyarrhythmia causing
1. Hypotension
2. Acutely altered mental status
3. Signs of shock
4. Ischemic chest discomfort
5. Acute heart failure
Monitor No
ACLS 2015

33. Yes
Atropine (0.5mg q 3-5min)
Transcutaneous pacing
Or
Dopamine infusion (2-20mcg/kg/min)
Or
Epinephrine infusion (2-10 mcg/min)
Consider expert consultation or
transvenous pacing

34. FIRST DEGREE HEART BLOCK
◦ PR interval prolonged but constant
◦ Rate and Rhythm may remain constant
◦ Causes – MI, Myocarditis/Endocarditis, Drugs, Hyperkalemia
◦ Usually asymptomatic; Monitor for progression to higher degree blocks

35. SECOND DEGREE AV BLOCK (MOBITZ
1)
◦ Ventricular rhythm irregular, Atrial rhythm regular
◦ PR interval prolongs with each cycle till a P wave appears without a QRS complex ; PR interval after the
non conducted P wave is shorter than the preceding one
◦ AKA Wenckebach’s phenomenon (Wenckebach – middle tract from SAN to AVN)
◦ Causes : Inferior wall MI (RCA blockage), Athletes
◦ T/t : Usually asymptomatic ; if occurring with IWMI – resolves in 48-72hrs
◦ Atropine - DOC

36. SECOND DEGREE HEART BLOCK (MOBITZ
II)
◦ 2:1 , 3:1, etc. pattern of conduction of Conducted: Non conducted P waves
◦ Ventricular rhythm irregular ; atrial rhythm regular
◦ PR interval constant in conducted QRS complexes
◦ Causes : (Below AV node) – Anterior MI (LCA blockage), Myocarditis, conduction system fibrosis
◦ t/t : Asymptomatic if ventricular rate is normal
◦ Close monitoring required – Temporary/permanent pacing may be necessary

37. 3RD DEGREE HEART BLOCK
(COMPLETE)
◦ Ventricular rhythm and atrial rhythm regular ; No relationship between the atrial and ventricular rhythms
◦ Ventricular rate is determined by the origin of the pacemaker
◦ No true PR interval exists
◦ Causes : Acute MI, Myocarditis, Fibrosis of conduction system
◦ Adam Stokes syndrome – sudden recurring episodes of loss of consciousness by transient interruption of cardiac
output by complete or incomplete heart block
◦ T/t – Atropine/Epinephrine ; Transcutaneous pacing

38. NON CONDUCTED PREMATURE ATRIAL
CONTRACTIONS
◦ Irregular rhythm because of missed ventricular contractions
◦ P wave occurred too early to be conducted (Too close to T wave)
◦ Causes : Acute coronary syndromes, Atrial enlargement, Digitalis toxicity, Emotional stress, Stimulants
◦ Treatment : Correct the underlying abnormality

39. SICK SINUS SYNDROME – ESCAPE
RHYTHM
◦ Ventricular rhythm is essentially regular
◦ Ventricular rate is 20-40 beats per minute
◦ P waves usually absent – may appear followed by QRS complexes
◦ QRS duration normal or prolonged ; T wave opposite to QRS complex
◦ Cause : SAN and AVN fail to generate an impulse
◦ T/t – Transcutaneous pacing

40. ATRIAL FIBRILLATION WITH SVR
◦ Ventricular rhythm is irregularly irregular
◦ Atrial rate is 300-600 beats/min ; Ventricular rate variable with varying RR interval
◦ No identifiable P waves; wavy baseline

41. APPROACH TO TACHYARRHYTHMIAS

42. SINUS TACHYCARDIA
◦ RR and PP intervals are regular
◦ Rate > 100/min ; Upper Ventricular rate = (220-age in years)/min
◦ PR interval and QRS duration normal
◦ Causes : Stimulants, Exercise, Fear, Fever, Hyperthyroidism, Infection, Nicotine, Pain, Shock
◦ T/t – Correct underlying pathology

43. MANAGEMENT OF
TACHYARRHYTHMIAS
Assess appropriateness of clinical situation
Heart rate > 150/min if tachyarrhythmia
Identify and treat underlying cause
• Maintain patent airway
• Oxygen
• Cardiac monitoring; BP and oximetry
Persistent tachyarrhythmia causing:
• Hypotension
• Acutely altered mental status
• Signs of shock
• Ischemic chest discomfort
• Acute heart failure
Synchronised
cardioversion
If regular narrow
complex -
Adenosine
Yes
ACLS 2015

44. Wide QRS? >0.12s
No
Yes
IV access and 12 lead ECG
• Adenosine if regular and
monomorphic
• Antiarrhythmic infusion
• Expert consult
IV access and 12 lead ECG
Vagal maneuvers
Adenosine if regular
Beta blocker or CCBs
Expert consult
Synchronised cardioversion
• Narrow regular : 50-100J
• Narrow irregular : 120-200J biphasic
or 200J Monophasic
• Wide regular : 100J
• Wide irregular : Defib dose
Adenosine
1st dose – 6mg with IV flush
2nd dose – 12mg
Antiarrhythmic infusions:
• Procainamide : 20-
50mg/min f/b 1-4mg/min
• Amiodarone : 150mg over
10mins f/b 1mg/min infusion
for 6hrs
• Sotalol : 100mg (1.5mg/kg)
over 5mins
No

45. SUPRAVENTRICULAR TACHYCARDIAS
◦ Regular rhythm
◦ Rate – 101-250/min
◦ P wave precedes QRS complex ; differ from sinus P waves based on the origin
◦ QRS duration < 0.11s (Narrow complex tachycardia)

46. CONTD.
Causes:
◦ Digitalis toxicity
◦ Electrolyte imbalance
◦ CAD, Cardiomyopathies
◦ Infection
◦ Pulmonary embolism
◦ Stimulants
Treatment:
◦ Adenosine – Slows rate of SAN, slows conduction via AVN –
abolishing Reentry circuits
◦ Onset – 10-40s
◦ Duration – 1-2mins
◦ Dose : 6mg IV push with 20mL saline; 12mg repeat dose
◦ Vagal maneuver – Carotid sinus massage
◦ Valsalva maneuver
◦ Synchronized Cardioversion

48. Atrio-Ventricular Nodal Reentrant Tachycardia
◦ Caused by a reentry circuit in or around the
AV node.
◦ The creation of two pathways forming the
re-entrant circuit – Slow and fast

50. AVNRT - ECG
◦ P waves are often hidden – being embedded in the QRS complexes.
◦ Pseudo r’ wave may be seen in V1
◦ Pseudo S waves may be seen in leads II, III or aVF.
◦ Results in a ‘typical’ SVT appearance with absent P waves and tachycardia

52. Atrio-Ventricular Reentrant Tachycardia

54. WOLFF PARKINSON WHITE
SYNDROME
◦ Pre excitation – a rhythm that originates above the ventricles and
transmits an impulse along a pathway outside the AV Node and
AV bundle.
◦ Regular rhythm unless associated with A fib
◦ Normal rate and P waves
◦ PR interval is shortened as the impulse travels very quickly across
the accessory pathway
◦ QRS > 0.12s; slurred upstroke of QRS complex (Delta wave)
◦ Pathway develops congenitally
◦ T/t – Usually asymptomatic ; synchronized cardioversion if
unstable
◦ Adenosine, CCBs and Beta blockers should be avoided –
slow AV nodal conduction and speed conduction via
accessory pathway

55. Dr. Louis Wolff
(American cardiologist)
Sir John Parkinson
(British Cardiologist)
Paul Dudley White
(American Cardiologist)

56. ATRIAL FLUTTER
◦ Atrial rhythm regular; ventricular rhythm regular or irregular (Narrow complex regular)
◦ Atrial rate 240 to 300 beats/min ; ventricular < 160 beats/min (AV nodal conduction rate)
◦ Saw Toothed Flutter waves present
◦ Causes : AT/A fib , Cardiac surgery, Cardiomyopathy, Digitalis/Quinidine toxicity, Hyperthyroidism
◦ T/t – Vagal maneuvers (unmask flutter), Beta blockers, CCBs, Sync. Cardioversion

58. ATRIAL FIBRILLATION
◦ Most common dysrhythmia
◦ No identifiable P waves, fibrillatory waves present; erratic, wavy baseline
◦ Ventricular rhythm irregularly irregular (Narrow complex irregular)
◦ Atrial rate 300-600/min ; Ventricular rate variable
◦ Predisposing Factors : CAD, DCMP, Heart failure, Hypertension, Rheumatic heart disease, Diabetes,
Hyperthyroidism, COPD, Antihistamines, LA toxicity
◦ T/t – Based on heart rate & presence of heart failure – CCBs, Beta blockers, Digoxin

59. MANAGEMENT OF ATRIAL
FIBRILLATION
AF with
FVR
Stable?
Unstable
• Cardioversion(100-200J)
• Anticoagulation
Workup
admit
Cardioversion fails
• Reattempt (Pre-treat with
ibultilide)
• Antiarrhythmic
(Procainamide/Amiodarone)
• Rate control
Candidate for
cardioversion?
• <48hrs
• New onset
• No LV dysfn
• No valvular ds
• No H/O VTE
• Therapeutic
anticoagulation
Sedation,
Synchronised
cardioversion

60. Accessory pathway? Anticoagulation if indicated
Cardioversion
(electric/pharmacological)
Avoid AV blocking drugs
Rate control
1. Calcium Channel Blockers (Diltiazem 0.25mg/kg)
2. Beta Blocker (Metoprolol 5mg Iv q5min x 3) – avoid in
asthma, COPD, ADHF
3. Digoxin 0.25-0.5mgIV (1st line in pts with ADHF)
4. Amiodarone (7mg/kg infusion)

61. Criteria Points
Gender Male 0
Female 1
Age <64 0
65-74 1
>75 2
Heart Failure 1
Hypertension 1
Diabetes mellitus 1
History of stroke, TIA,
or thromboembolism
2
Vascular disease 1
CHA2DS2-VASc score
◦ ≥2 : Chronic anticoagulation with Warfarin (INR 2-3)
or Apixaban/Dabigatran/Rivaroxaban/Edoxaban
◦ 1: Conflicting evidence – Age 65-74yrs is a strong
predictor to start anticoagulation
◦ 0 : No anticoagulant therapy
For the rare patient who cannot take anticoagulant
therapy for reasons other than bleeding risk, we
suggest aspirin 75 to 100 mg daily plus clopidogrel 75
mg daily
Stroke Prevention in Atrial Fibrillation Study. Circulation. 1991;84(2):527

62. MONOMORPHIC VT
◦ Essentially Regular ventricular rhythm
◦ P waves not seen; If seen no relationship with QRS complexes
◦ Ventricular rate 101-250/min ; QRS – Wide complex (mostly) regular(mostly)
◦ Causes – Acid base imbalance, ACS, Cardiomyopathy, Stimulant abuse, Electrolyte imbalance
(hypo/hyperkalaemia), Myocardial contusion, TCA overdose
◦ T/t – CPR and defibrillation for pulseless VT ; Ventricular antiarrhythmics(Procainamide, Sotalol,
Amiodarone) for stable patients ; Synchronised cardioversion for unstable patients

63. POLYMORPHIC VT
◦ Ventricular rhythm maybe irregular or regular(rare)
◦ Ventricular rate 150-300/min
◦ No P waves
◦ Alteration in the amplitude and direction of QRS complexes – Wide Irregular QRS
◦ Torsades de Pointes – Polymorphic VT in the presence of long QT interval
◦ Causes – Same as MVT
◦ T/t – Same as MVT

64. VENTRICULAR FIBRILLATION
◦ Rapid and chaotic rhythm with no pattern or regularity
◦ No discernible P, QRS waves
◦ Causes : ACS, Electrolyte disturbances, Electrocution, Antiarrhythmic overdose, Severe heart failure
◦ T/t – High quality CPR and defibrillation (Shockable rhythm)

65. MULTIFOCAL ATRIAL TACHYCARDIA
◦ Multiform Atrial Rhythm/Wandering pacemaker – Rhythm, size, shape and direction of P waves vary
(at least 3 different P waves in the same lead)- Transitional rhythm
◦ Irregular rhythm – Pacemaker is ectopic atrial locations
◦ P waves vary in size and shape ; PR interval varies
◦ QRS complex normal or narrow
◦ Causes – Severe COPD ; ACS, Valvular heart disease, Hypomagnesemia, precursor of A fib
◦ T/t – correct underlying cause

66. PREMATURE ATRIAL COMPLEXES
◦ Premature Beats can be:
◦ Premature atrial complexes
◦ Premature junctional complexes
◦ Premature ventricular complexes
◦ Patterns may exist :
◦ Couplet – 2 premature beats in a row
◦ Bursts/runs – 3 or more premature beats in a row
◦ Bigeminy – Every other beat is a premature beat
◦ Trigeminy – every 3rd beat is a premature beat
◦ Quadrigeminy – every 4th beat is a premature beat

67. PAC:
• Irregular rhythm because of early beats
• Premature P waves , often differing in
shape with normal p waves
• Often not followed by or followed by an
incomplete compensatory pause
PVC:
• Irregular rhythm
because of premature
beats
• P wave usually absent
before the PVC and may
occur after QRS

68. MYOCARDIAL
ISCHEMIA

69. BLOOD SUPPLY OF THE HEART
Anterior wall
(V3,V4)
Septum
(V1,V2)
Lateral Wall
(I,aVL,V5,V6)
Inferior wall
(II,III, aVF)
Inferior wall
(II,III,avF)
Inferobasal/Posterior
(V7,V8,V9 – indicative
V1,V2,V3 – reciprocal)
Right ventricle

70. ELECTRO-ANATOMICAL
RELATIONSHIP

71. PROGRESSION OF ECG CHANGES

72. ELECTROPHYSIOLOGY OF MI
◦ Normally – ST segment is isoelectric – corresponding to Plateau phase of Cardiac action potential
◦ Severe, acute ischemia - lowers the resting membrane potential ; shortens the duration of the
action potential; changes the shape of the plateau (phase 2) of the action potential in the ischemic
area - voltage gradient between normal and ischemic zones - current flow between these regions
during both systolic and diastolic portions of the cycle - currents of injury
◦ Transmural (severe acute) MI - ST vector is shifted in the direction of the outer (epicardial and
subepicardial) layers – ST elevation - pathologic early (accelerated) repolarization causes the
outside surface of ischemic cells to become positively charged relative to nonischemic cells, which
are still in a depolarized state (negative charge outside)
◦ Sub endocardium - systolic ST vector typically shifts toward the inner ventricular layer and the
ventricular cavity, while the diastolic injury vector points toward the epicardium, that is, the
opposite of the directions observed with transmural (epicardial) ischemia – ST depression

73. DIAGNOSIS OF STEMI - ECG
◦ New ST elevation at the J point in two contiguous leads of >0.1 mV in all leads other than leads
V2-V3
◦ For leads V2-V3 the following cut points apply: ≥0.2 mV in men ≥40 years, ≥0.25 mV in men
<40yrs and women
Other conditions which are treated as a STEMI
◦ New or presumed new LBBB
◦ Isolated posterior MI
Practice Guidelines 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction

74. ANTERIOR INFARCTION
◦ Anterior wall MI mostly occurs due to LAD occlusion – this seems like an Anteroseptal MI
◦ Leads V1-V4 involved ; Reciprocal changes in III ,aVF
◦ Poor R wave progression is noted
◦ Transition zone is at V5 – R wave exceeds S wave amplitude

75. LATERAL INFARCTION
◦ Involvement of leads I, aVL, V5, V6 (here V4 also) – ST elevation
◦ Reciprocal changes in III, aVF
◦ Isolated lateral infarction is usually associated with Circumflex artery occlusion

76. INFERIOR INFARCTION
◦ Involvement of leads II, III, aVF – ST elevation
◦ Reciprocal changes in aVL, V1, V2 ( suggesting inferobasal involvement)
◦ Mostly due to involvement of Posterior descending branch of RCA

77. PERICARDITIS
◦ Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL,
aVF) and precordial leads (V2-6).
◦ Reciprocal ST depression and PR elevation in lead aVR (± V1).
◦ Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.

78. CHAMBER
ENLARGEMENT
Hypertrophy or Dilatation

79. ATRIAL ENLARGEMENTS
◦ First half of P wave corresponds to SAN stimulating
the Right atrium.
◦ The downslope of the P wave reflects stimulation of
Left atrium.
◦ Right atrial abnormality – COPD with/without
Pulmonary Hypertension, Right ventricular failure
◦ Left Atrial abnormality – CAD, Cardiomyopathies,
Hypertensive heart disease, Valvular heart disease

80. VENTRICULAR ABNORMALITIES
◦ RVH – Since Muscle mass of RV is less than LV, it must be extremely enlarged for ECG changes
◦ Tall R waves in V1-V3 ; Deeper than normal S waves in I, aVL, V5 and V6
◦ RVH causes – Pulmonary HTN, Valvular heart disease, COPD

81. LEFT VENTRICULAR HYPERTROPHY
◦ Increased QRS amplitude and changes in
the ST-T
◦ R waves in leads I, aVL, V5, V6 are taller
; S waves in V1 and V2 are deeper than
normal
◦ QRS duration increased
◦ Causes- Hypertension, Hypertrophic
cardiomyopathy, AS, AR
◦ Cornell Voltage criterion:
◦ S wave amplitude (V3) + R wave
amplitude (aVL)
◦ >20mm(women) or >28mm(men) suggests
LVH

82. ELECTROLYTE
ABNORMALITIES

84. HYPOKALEMIA
◦ ST segment depression
◦ Decrease in T wave amplitude
◦ Prominent U waves – amplitude of U waves exceed T waves
◦ P wave amplitude and duration are progressively increased
◦ Prolongation of PR interval
◦ Increased QRS duration with severe Hypokalemia

85. HYPERCALCEMIA
◦ Shortening of the ST segment
◦ Decreased QT interval duration
◦ Osborn wave – Positive deflection of the J point (Negative in aVR and V1) – also seen in Hypothermia

86. HYPOCALCEMIA
◦ Lengthening of the ST segment
◦ Increased QT interval duration

87. DIGITALIS TOXICITY
Digoxin effect:
◦ Down sloping ST depression with a
characteristic “Salvador Dali sagging”
appearance
◦ Flattened, inverted, or biphasic T waves.
◦ Shortened QT interval.
Arrhythmias :
◦ supraventricular tachycardia
◦ slow ventricular response
◦ PVCs, Sinus bradycardia, slow atrial fibrillation,
AV blocks, AF, Vtach

88. SALVADOR DALI

89. BUNDLE BRANCH BLOCKS
◦ A Bundle branch block is a disruption in the impulse conduction from Bundle of His
through either the right or left bundle branch to the Purkinje fibres.
◦ Right bundle branch – single, long, thin
◦ Left bundle branch – Anterior, Posterior and Middle (some) fascicles
◦ For suspicion of Bundle branch block :
1. QRS must have an abnormal duration (0.12s or greater) – wide QRS in complete block
2. QRS complex must arise because of supraventricular activity

90. RIGHT BUNDLE BRANCH
◦ Septal depolarization – Left to right – small positive deflection in V1 (R)
◦ rSR’ pattern is characteristic of RBBB – AKA “M” or “Rabbit ear” pattern

91. LEFT BUNDLE BRANCH BLOCK
◦ The septum and LV is depolarized by right bundle branch – net movement of current away from V1 –
negative deflection
◦ Deep negative deflection (S) wave due to large muscle mass of LV

92. PACEMAKER RHYTHMS
◦ A cardiac pacemaker is a battery powered device that delivers an electric current to the heart to
stimulate depolarization.
◦ Components :
1. Pulse generator – Power source
2. Pacing lead – carries electrical impulse from the pacemaker to the heart
3. Sensing lead – carries information from the heart to the pacemaker (usually the same as the
pacing lead)
◦ Triggering
◦ Inhibition

93. IMPLANTABLE CARDIOVERTER
DEFIBRILLATORS
Tiered (staged) Dysrhythmia therapy:
◦ Capable of delivering staged therapy in treating
VT and VF.
1. Anti-tachycardia Pacing
2. Cardioversion shocks – VT
3. Defibrillation shocks – VF
Indications :
◦ Drug refractory VF / Sustained VT
◦ Congenital Long QT syndrome

94. BIPOLAR VS UNIPOLAR PACING
◦ Bipolar system contains a positive and negative electrode at the distal tip of pacing wire
◦ Unipolar system has one pacing electrode – negative electrode outside the heart in contact with pulse generator
◦ Bipolar pacing spike is smaller than unipolar system because of shorter distance between positive and negative
electrode

95. ATRIAL VS VENTRICULAR PACING
Single chamber pacemakers – One lead placed
in the heart
• Atrial (RA)
• Ventricular (RV)
Dual chamber pacing – One lead in RA and
other in RV
Aka Physiologic pacing
The PR interval is called Atrioventricular interval

96. PROBLEMS WITH PACEMAKERS
Failure to Pace: Inability of pacemaker to depolarize
myocardium
• Battery failure
• Displacement or fracture of tip
• Pulse generator failure
• Broken/loose connection
• Electromagnetic interference
Failure to Capture : Inability of artificial
pacemaker to depolarize the Myocardium
• Displacement of lead wire
• Output energy low
• Battery failure
• Edema/scar at electrode tip
• Increased threshold due to electrolyte
imbalance

97. PREOPERATIVE ECG
◦ Obtained in patients with known cardiovascular disease, significant arrhythmia, peripheral arterial
disease, cerebrovascular disease or significant structural heart disease (unless undergoing a low
risk procedure).
◦ Can also be considered in patients undergoing high risk surgeries (Risk of MACE >1%)
◦ Purpose : Baseline ECG for comparison
◦ The ECG should be evaluated for :
◦ Presence of prominent Q waves or significant ST-segment deviation
◦ Chamber abnormality/hypertrophy
◦ QTc prolongation
◦ Bundle branch block (BBB)
◦ Arrhythmias
2014 ACC/AHA Guidelines

98. RECOMMENDATIONS
Warrants CANCELLATION of case:
◦ Acute axis deviation
◦ New bundle branch block (BBB)
◦ Acute ST-elevation myocardial infarction
(STEMI) or acute pericarditis
◦ Acute ST-segment depression in multiple
leads
◦ Mobitz Type II atrioventricular (AV) block
or third degree AV block
◦ Tall peaked T waves
◦ Prolongation of the corrected QT (QTc)
interval
◦ Narrow complex supraventricular
tachyarrhythmias
◦ Wide complex tachycardia
Not necessary to postpone surgery:
◦ Left ventricular hypertrophy (LVH) due to
chronic hypertension, AS, Hypertrophic
cardiomyopathy
◦ Sinus bradycardia with a rate >45/min, 1st
Degree AV block, Mobitz type 1 block

99. THANK YOU!
SOURCES :
• LIFTL
• ACLS
• ECG MADE EASY
(BARBARA AEHLERT)
• THE ECG MADE EASY
(HAMPTON)
• ‘CIRCULATION’ JOURNALS
• ‘HEART’ JOURNALS
• HARRISON’S INTERNAL
MEDICINE
• UPTODATE