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Transcript
ECG Analysis (Fundamentals)
Vukiet Tran, MD, MBA
ACTIVITY DISCLAIMER
The material presented here is being made available by the American Academy of Family
Physicians for educational purposes only. This material is not intended to represent the
only, nor necessarily best, methods or procedures appropriate for the medical situations
discussed. Rather, it is intended to present an approach, view, statement, or opinion of the
faculty, which may be helpful to others who face similar situations.
The AAFP disclaims any and all liability for injury or other damages resulting to any
individual using this material and for all claims that might arise out of the use of the
techniques demonstrated therein by such individuals, whether these claims shall be
asserted by a physician or any other person. Every effort has been made to ensure the
accuracy of the data presented here. Physicians may care to check specific details such as
drug doses and contraindications, etc., in standard sources prior to clinical application. This
material might contain recommendations/guidelines developed by other organizations.
Please note that although these guidelines might be included, this does not necessarily
imply the endorsement by the AAFP.
DISCLOSURE
It is the policy of the AAFP that all individuals in a position to control content disclose any relationships
with commercial interests upon nomination/invitation of participation. Disclosure documents are reviewed
for potential conflict of interest (COI), and if identified, conflicts are resolved prior to confirmation of
participation. Only those participants who had no conflict of interest or who agreed to an identified
resolution process prior to their participation were involved in this CME activity.
All individuals in a position to control content for this activity have indicated they have no relevant
financial relationships to disclose.
The content of my material/presentation in this CME activity will not include discussion of unapproved or
investigational uses of products or devices.
The content of my material/presentation in this CME activity will include discussion of unapproved or
investigational uses of products or devices as indicated:
Vukiet Tran, MD, MBA
Assistant Professor, Department of Family and Community Medicine,
University of Toronto, Ontario, Canada.
Dr. Tran practices family medicine and emergency medicine in a group
practice in suburban Toronto, Ontario, Canada. His practice
encompasses the full spectrum of family medicine, from pediatric
patients to the elderly. Dr. Tran has taught for 15 years in an academic
emergency medicine center affiliated with the University of Toronto. His
specialty topics include emergency medicine, cardiovascular medicine,
dermatology, and procedures in the emergency department. Dr. Tran
believes in lifelong learning.
Learning Objectives
1.
Compare and contrast the findings of ECG tests in different patient
cases.
2.
Relate the implications of ECG readings to potential cardiac
disease.
3.
Compare the findings of an ECG to a patient’s clinical
presentation.
4.
Compare the results of multiple ECG findings from the same
patient.
ECG IS ONLY A TOOL TO
SUPPLEMENT YOUR CLINICAL
ASSESSMENT
INTERPRETATION OF ECG MUST
BE DONE SYSTEMATICALLY
- ESSENTIAL COMPONENTS
NEED TO BE SYNTHESIZED
- THE GOAL IS A RAPID AND
ACCURATE DIAGNOSIS
Simple and tried process
1.
2.
3.
4.
5.
6.
7.
Rate
Rhythm
Axis
Intervals
ST segments
Morphology
Special conditions
Simple and tried process
1.Rate
2.
3.
4.
5.
6.
7.
Rhythm
Axis
Intervals
ST segments
Morphology
Special conditions
Normal ECG paper
Pacemaker sites of the heart
Pacemaker
Normal rate (bpm)
Sinoatrial (SA) node
60-100
Atrioventricular node (Junctional)
40-60
Ventricular
20-40
Determining the rate
• Method I: 300-150-100-75-60-50-42-38 rule
–
–
–
–
Choose an R that falls on or close a thick line
The first thick line right to it is 300 line
The second is the 150 line
And so on…
OR
– Start with a QRS that occurs on a thick line
– Locate the next QRS
– Divide 300 by the number of thick lines in between the QRSs
1
2
Determining the rate
• Method II: count the number of QRS in 6
seconds
– That number multiple by 10
– More accurate method if the rhythm is
irregular
3
4
Determining the rate
• Method III: duration between two R waves
– Count in duration (in seconds) between two R
waves
– divide 60 by this number
5
0.68 sec
Rate = 60 ÷ 0.68 = 88
Simple and tried process
1. Rate
2.Rhythm
3.
4.
5.
6.
7.
Axis
Intervals
ST segments
Morphology
Special conditions
Sinus rhythms
• Normal Sinus
6
Normal Sinus Rhythm
• Regular rhythm 60-100
• Each QRS are preceded by a normal P
wave
• Each P wave followed by a QRS Complex
• P are positives in I, II, AVF
• PR interval is normal
Sinus rhythms
• Sinus Bradycardia
7
Sinus rhythms
• Sinus Tachycardia
8
Junctional rhythms
• Junctional escape rhythm
9
Junctional rhythm
• Rate of 40-60
• QRS are narrow
• No P waves
Ventricular rhythms
• Idioventricular escape rhythm
10
Ventricular rhythm
•
•
•
•
Rate between 20-40
Regular rate
QRS are wide
No P waves
Accelerated Idioventricular 10A
Simple and tried process
1. Rate
2. Rhythm
3.Axis
4.
5.
6.
7.
Intervals
ST segments
Morphology
Special conditions
Normal QRS Axis
Axis determination
• Method I
– Determine which quadrant your axis is in using Lead I
and AVF
• Method II
– Find the most isoelectric lead (the Axis is
perpendicular to this lead)
• Method III
– The tallest QRS points toward the Axis (Limb Leads)
Axis – Method I
Lead I +ve
Lead AVF +ve
Axis Method II
11
Axis Method III
11
Causes of Abnormal Axis
QRS Axis
Possible Cardiac Etiologies
Noncardiac Etiologies
Normal
Normal condition
Left (-30 to -90)
LVH – Left Ventricular Hypertrophy
LAFB – Left Anterior Fascicular Block
VT – Ventricular Tachycardia
LBBB – Left Bundle Branch Block
Inferior wall MI
Pneumothorax (mechanical shift)
Right (+110 to +
180)
Normal young adult and pediatric patients
RVH – Right Ventricular Hypertrophy
LPFB – Left Posterior Fascicular Block
VT – Ventricular Tachycardia
Dextrocardia
Lateral wall MI
COPD and Cor Pulmonale
Acute PE
Hyperkalemia
Extreme Left (-90
to -180)
COPD
Dextrocardia
Right axis deviation
• Left posterior fascicular block
• Hyperkalemia
• Na2+ channel blocking drugs (e.g. TCA’s, Quinidine & Antiarrhythmics)
• Right ventricular hypertrophy
• Pulmonary HTN - Acute (PE) and chronic (COPD) lung disease
• Ventricular ectopy (VT)
• Lateral MI (from Q-waves in lead I)
• Lead misplacement
• Dextrocardia
• Normal thin adults with horizontally positioned hearts
Simple and tried process
1. Rate
2. Rhythm
3. Axis
4.Intervals
5. ST segments
6. Morphology
7. Special conditions
Normal intervals
Intervals
Normal range
PR
0.12 - 0.20 seconds (rate dependent)
QRS
< 0.10 seconds
QT
< 450 msec in men
< 470 msec in women
Rate dependent
Age dependent
Bazett formula
QTc = QT interval/√R-R interval
12
PR intervals
13
PR Intervals
14
QRS intervals
15
QT intervals
16
QT intervals
17
QT interval
QT interval
Calculations
Assessment of QT interval
Causes of QT prolongation
• Long QT Syndrome
– Congenital
– Acquired
• Medication
• Electrolyte imbalance
• Ischemia
Drugs
associated with
prolonged QT
Simple and tried process
1.
2.
3.
4.
Rate
Rhythm
Axis
Intervals
5.ST segments
6. Morphology
7. Special conditions
ST Segment deviations
ST Segment deviations
18
ST Segment deviations
19
ST Segment deviations
20
ST Segment deviations
21
ST Segment deviations
22
ST Segment deviations
23
ST Segment deviations
24
ST Segment deviations
25
ST Segment deviations
26
ST Segment deviations
27
ST Segment deviations
28
ST Segment deviations
29
STEMIs
Territory
Leads
Coronary involved
Anterior
STE V1-V4
LAD
Lateral
STE V3-V6, I, AVL
Marginal branch off Cx or
Diagnonal off LAD
Septal
STE V1-V4
LAD – septal branch
Inferior
STE II, III, AVF
RCA (80%) or dominant left Cx
(20%)
Posterior
Big R in V1-V3
STD in V1-V3
STE in V8-V9
Associated with Inferior MI
Cx
Right ventricle
STD in V1-V3
STE in V4r
Associated with Inferior MI
RCA
Inferior MI
• Hallmark findings:
– STE II, III, AVF
– ST depression in AVL
– ALWAYS look for concurrent RV MI
• STE V1 and/or STDV5,V6
– Get a RIGHT sided EKG (15-lead)
• STE-> V4R
Inferior/Right sided MI
• Be careful with MONA!!
RV MI
•
•
•
•
•
Most occur concurrent with inferior MI
Remember to get the RIGHT sided EKG!
Isolated STE V1 on the routine EKG
STE in V4R
RV MI is often associated with significant
hypotension (preload dependence)
Posterior MI
• In V1-V3
– Horizontal ST depression
– Tall, broad R waves (>30ms)
– Upright T waves
– Dominant R wave (R/S ratio > 1) in V2
Ddx of ST elevations
•
•
•
•
•
•
•
•
1-STEMI’s
2-LV Aneurysms
3-LVH
4-LBBB
5-RBBB
6-Paced
7-Pericarditis
8-Early Repolarization
Summary
Territory
Leads
Coronary involved
Anterior
STE V1-V4
LAD
Lateral
STE V3-V6, I, AVL
Marginal branch off Cx or
Diagnonal off LAD
Septal
STE V1-V4
LAD – septal branch
Inferior
STE II, III, AVF
RCA (80%) or dominant left Cx
(20%)
Posterior
Big R in V1-V3
STD in V1-V3
STE in V8-V9
Associated with Inferior MI
Cx
Right ventricle
STD in V1-V3
STE in V4r
Associated with Inferior MI
RCA
Simple and tried process
1.
2.
3.
4.
5.
Rate
Rhythm
Axis
Intervals
ST segments
6.Morphology
7. Special conditions
Left Ventricular Hypertrophy (LVH)
LVH, no strain
•
•
•
•
S in Lead V1 or V2 + R in V5 or V6>35
R in AVL > 11
R in V5 or V6 > 27
Repolarization changes
30
LVH with strain
31
RVH
Right Ventricular Hypertrophy
32
• R > S in V1
• R in V1 + S in V6 > 11
• Right axis > 90o
• Repolarization changes
Bundle Branch Blocks
Left Bundle Branch Blocks
Left Bundle Branch Block 33
• No Q I, AVL, V6
• RSR1
• QRS predominantly
negative in V1
• QRS>0.12
• Repolarization
changes
Right Bundle Branch Blocks
Right Bundle Branch Block 34
• QRS>0.12
• RSR1 lead V1
• QRS predominantly
positive in V1
• Wide S in I
• Repolarization
changes
U wave
U Wave
• Positive deflection that
occasionally appears after the
T wave
• It presence or absence does
not signify a pathologic
process
– Certain disease state make
the U wave more
prominent
Medical conditions
•
•
•
•
•
•
•
Hypokalemia
Hypocalcemia
Hypomagnesemia
Hypothermia
Raised ICP
LVH
Hypertrophic cardiomyopathy
Drugs
•
•
•
•
Digoxin
Phenothiazines
Class Ia antiarrhythmics (Quinidine,
Procainamide)
Class III antiarrhythmics (Amiodarone, Sotalol)
U-Wave
35
J wave
J wave
36
Simple and tried process
1.
2.
3.
4.
5.
6.
7.
Rate
Rhythm
Axis
Intervals
ST segments
QT interval
Morphology
8.Special conditions
Normal variants
1. Benign Early Repolarization
2. Athlete’s Heart
3. Persistent Juvenile Pattern
Early Repolarization
• STE beginning at the J point
• STE is minimal (< 2mm)
• Upward concave morphology,
particularly at the initial portion
of the ST segment
• Diffusely distributed, mainly
V2-V6
• T waves are “peaked”
Early Repolarisation
37
Athlete’s Heart
• Sinus bradycardia
• 1st AV or 2nd AV block (Mobitz I)
• Increased R or S voltage
• Benign early repolarisation
• Deep Q wave in inferior leads
Athlete’s Heart
38
Persistent Juvenile Pattern
• Healthy children and young
adults
• Women >>> men
• < 40-45 yo
• DDx:
– Wellens’ disease
– Ischemia
– PE
Persistent Juvenile Pattern
39
Arrhythmias and Dysrrhythmias
DO YOU HAVE AN APPROACH TO
TACHYARRHYTHMIAS?
Approach to Tachy-arrhythmias
• Is it Regular or Irregular?
• Is it Narrow or Wide Complex?
• What is the relationship of the P to the
QRS?
48
Regular or
Irregular?
49
50
51
52
53
Irregularly irregular rhythms
•
•
•
•
•
Premature atrial or ventricular beats
Sinus arrhythmia
Multifocal atrial tachycardia
Atrial fibrillation
Atrial flutter
Approach to Tachy-arrhythmias
OR
Categories of Arrhythmias
Supraventricular tachycardias
54
Where are
the Ps?
55
Approach to Tachy-arrhythmias
• Is it regular or irregular?
• Is it narrow or wide complex?
• What is the relationship of the P to the
QRS?
Summary
of tachyarrhythmias
Regular and Narrow
Irregular and Narrow
Sinus Tachycardia
Atrial Flutter with fixed bloc
Paroxysmal Atrial Tachycardia with block
SVT
Regular and Wide
Sinus Arrhythmia
Extrasystole
Atrial Fibrillation
Atrial Flutter with variable bloc
Paroxysmal Atrial tachycardia (PAT)
MAT (Multifocal Atrial Tachycardia)
At least 3 different P waves, one for each QRS
Irregular and Wide
Above, with aberrancy
Above, with aberrancy
Hyperkalemia
Drug Toxicity
VT
Ventricular Flutter
Hyperkalemia
Drug Toxicity
Ventricular Tachycardia
Torsade
VF
What rhythm is this?
40
What rhythm is this?
41
What rhythm is this?
43
What rhythm is this?
45
How would you treat this patient?
56
How would you treat this patient?
58
How would you treat this patient?
59
How would you treat this patient?
60
Most important question!
Not perfusing
Perfusing
Narrow complex
Narrow complex
Synchronized cardioversion
Adenosine
Calcium Channel Blockers
Beta-Blockers
Digoxin
Wide complex
Wide complex
Synchronized cardioversion (VT)
Defibrillation (VF)
Procainamide
Amiodarone
Synchronized cardioversion
Management
Rhythm
Approach
Sinus Tachycardia
Treat the cause
Premature beats
Treat the cause
Multifocal atrial tachycardia (MAT)
Treat the cause
SVT
Chemical cardioversion
•
Adenosine
•
Calcium channel blockers
•
Beta-blockers
Electrical cardioversion if unstable
Atrial fibrillation or flutter
Rate control
•
Adenosine
•
Calcium channel blockers
•
Beta-blockers
Rhythm control
•
If < 48h only
Anticoagulation
Electrical cardioversion if unstable
Test
61
Test
63
Test
64
Regular and Narrow
Sinus Tachycardia
Atrial Flutter with fixed block
Atrial tachycardia/SVT
P with every QRS
Sinus Tachycardia
P not with every QRS
No P with QRS
A. Flutter with fixed block
SVT
Regular and wide
Sinus Tachycardia
Atrial Flutter with fixed bloc
SVT
Hyperkalemia
Drug Toxicity
VT
Ventricular Flutter
Aberrancy
Irregular and Narrow
Sinus Arrhythmia
Extrasystole
Atrial Fibrillation
Atrial Flutter with variable bloc
MAT (Multifocal Atrial Tachycardia)
PAT
Drug toxicity
1 extra beat
Extrasystole
P with every
QRS
P with every
QRs, but
different
Not every P
conducts a
QRS
SA
MAT
Afib or Flutter
Regular and wide
Sinus Arrhythmia
Extrasystole
Atrial Fibrillation
Atrial Flutter with variable bloc
MAT (Multifocal Atrial Tachycardia)
Hyperkalemia
Drug toxicity
Afib or Flutter with Pre-excitation
Ventricular Tachycardia
Torsade
VF
Aberrancy
Summary of tachyarrhythmias
Regular and Narrow
Sinus Tachycardia
Atrial Flutter with fixed bloc
Paroxysmal Atrial Tachycardia with block
SVT
Regular and Wide
Irregular and Narrow
Sinus Arrhythmia
Extrasystole
Atrial Fibrillation
Atrial Flutter with variable bloc
Paroxysmal Atrial tachycardia (PAT)
MAT (Multifocal Atrial Tachycardia)
At least 3 different P waves, one for each QRS
Irregular and Wide
Above, with aberrancy
Above, with aberrancy
Hyperkalemia
Drug Toxicity
VT
Ventricular Flutter
Hyperkalemia
Drug Toxicity
Ventricular Tachycardia
Torsade
VF
QUESTIONS?
DO YOU HAVE AN APPROACH
FOR BRADYARRHYTHMIAS?
Approach to Brady-arrhythmias
• Is the patient
stable?
Approach to Brady-arrhythmias
• Not stable?
• Transcutaneous or transvenous Pacemaker
Drugs
• Dopamine
• NorEpineprhine
• Epinephrine
Heart blocks - Summary
Type
Characteristics
Hemodynamic impact
1st
PR longer than 0.20
None
Mobitz 1
PR progressively prolongs, then P drops a QRS
There is a junctional or ventricular escape beat
Min-mod
Mobitz 2
PR consistently stays identical, then P drops a QRS
There is a junctional or ventricular escape beat
Mod-severe
Atrial and ventricular rates are independent of one another
There is a junctional or ventricular escape beat
Mod-severe
2nd
3rd
Approach to Brady-arrhythmias
• Is the patient stable?
• What is the rate?
• Are there P waves?
• Are the QRS wide?
What rhythm is this?
46
1st degree AV block
65
2nd degree AV Block – Mobitz I
66
Wenckebach , Lateral Ischemia 67
Second Degree Type II 2:1 block, RBBB
68
3rd degree AV block
69
3rd Degree AV Block, LVH
70
Heart blocks - Summary
Type
Characteristics
Hemodynamic impact
1st
PR longer than 0.20
None
Mobitz 1
PR progressively prolongs, then P drops a QRS
There is a junctional or ventricular escape beat
Min-mod
Mobitz 2
PR consistently stays identical, then P drops a QRS
There is a junctional or ventricular escape beat
Mod-severe
Atrial and ventricular rates are independent of one another
There is a junctional or ventricular escape beat
Mod-severe
2nd
3rd
Sinus arrhythmia
•
•
•
•
P wave does not vary
P-P interval varies
Usually dependent on respiration
If independent of respiration, more
commonly pathologic, but may be
inconsequential.
71
Sinus pause/arrest
• Temporary failure of impulse generation:
pause
• If prolonged: arrest
72
73
Accelerated idioventricular rhythm
• Focus is in the His-bundle branch system
or ventricular myocardium
• Regular
• Rate faster than usual slow idioventricular
rhythms
74
SUMMARY
Summary of tachyarrhythmias
Regular and Narrow
Sinus Tachycardia
Atrial Flutter with fixed bloc
Paroxysmal Atrial Tachycardia with block
SVT
Regular and Wide
Irregular and Narrow
Sinus Arrhythmia
Extrasystole
Atrial Fibrillation
Atrial Flutter with variable bloc
Paroxysmal Atrial tachycardia (PAT)
MAT (Multifocal Atrial Tachycardia)
At least 3 different P waves, one for each
QRS
Irregular and Wide
Above, with aberrancy
Above, with aberrancy
Hyperkalemia
Drug Toxicity
VT
Ventricular Flutter
Hyperkalemia
Drug Toxicity
Ventricular Tachycardia
Torsade
VF
Most important question!
Not perfusing
Perfusing
Narrow complex
Narrow complex
Synchronized cardioversion
Adenosine
Calcium Channel Blockers
Beta-Blockers
Digoxin
Wide complex
Wide complex
Synchronized cardioversion (VT)
Defibrillation (VF)
Procainamide
Amiodarone
Synchronized cardioversion
Management
Rhythm
Approach
Sinus Tachycardia
Treat the cause
Premature beats
Treat the cause
Multifocal atrial tachycardia (MAT)
Treat the cause
SVT
Chemical cardioversion
•
Adenosine
•
Calcium channel blockers
•
Beta-blockers
Electrical cardioversion if unstable
Atrial fibrillation or flutter
Rate control
•
Adenosine
•
Calcium channel blockers
•
Beta-blockers
Rhythm control
•
If < 48h only
Anticoagulation
Electrical cardioversion if unstable
Thank You
Questions?
[email protected]
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