DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What is an EKGbullThe electrocardiogram (EKG) is a representation of the electrical events of the cardiac cyclebullEach event has a distinctive waveform bullthe study of waveform can lead to greater insight into a patientrsquos cardiac pathophysiology

mclmal

V1

V1

V2

V2

V3

V3

V4

V4

V5V5

Horizontal plane - the six chest leads

V6

V6RA

LALV

RV

65

9

The 12-LeadsThe 12-leads include

ndash3 Limb leads (I II III)

ndash3 Augmented leads (aVR aVL aVF)

1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50

ndash6 Precordial leads (V1- V6)

1938 -AHA and Cardiac society of great Britain

1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize

60 ndash 100 times a minute

40 ndash 60 times a minute

20 ndash 40 times a minute

Pacemakers of the heart

1111

Cardiac Conduction

>

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

What is an EKGbullThe electrocardiogram (EKG) is a representation of the electrical events of the cardiac cyclebullEach event has a distinctive waveform bullthe study of waveform can lead to greater insight into a patientrsquos cardiac pathophysiology

mclmal

V1

V1

V2

V2

V3

V3

V4

V4

V5V5

Horizontal plane - the six chest leads

V6

V6RA

LALV

RV

65

9

The 12-LeadsThe 12-leads include

ndash3 Limb leads (I II III)

ndash3 Augmented leads (aVR aVL aVF)

1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50

ndash6 Precordial leads (V1- V6)

1938 -AHA and Cardiac society of great Britain

1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize

60 ndash 100 times a minute

40 ndash 60 times a minute

20 ndash 40 times a minute

Pacemakers of the heart

1111

Cardiac Conduction

>

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

mclmal

V1

V1

V2

V2

V3

V3

V4

V4

V5V5

Horizontal plane - the six chest leads

V6

V6RA

LALV

RV

65

9

The 12-LeadsThe 12-leads include

ndash3 Limb leads (I II III)

ndash3 Augmented leads (aVR aVL aVF)

1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50

ndash6 Precordial leads (V1- V6)

1938 -AHA and Cardiac society of great Britain

1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize

60 ndash 100 times a minute

40 ndash 60 times a minute

20 ndash 40 times a minute

Pacemakers of the heart

1111

Cardiac Conduction

>

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

V1

V1

V2

V2

V3

V3

V4

V4

V5V5

Horizontal plane - the six chest leads

V6

V6RA

LALV

RV

65

9

The 12-LeadsThe 12-leads include

ndash3 Limb leads (I II III)

ndash3 Augmented leads (aVR aVL aVF)

1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50

ndash6 Precordial leads (V1- V6)

1938 -AHA and Cardiac society of great Britain

1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize

60 ndash 100 times a minute

40 ndash 60 times a minute

20 ndash 40 times a minute

Pacemakers of the heart

1111

Cardiac Conduction

>

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

9

The 12-LeadsThe 12-leads include

ndash3 Limb leads (I II III)

ndash3 Augmented leads (aVR aVL aVF)

1942- Goldberger increased Wilsonrsquos Unipolar lead voltage by 50

ndash6 Precordial leads (V1- V6)

1938 -AHA and Cardiac society of great Britain

1906 - William Einthoven diagnoses some heart problems 1924 - the noble prize

60 ndash 100 times a minute

40 ndash 60 times a minute

20 ndash 40 times a minute

Pacemakers of the heart

1111

Cardiac Conduction

>

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

60 ndash 100 times a minute

40 ndash 60 times a minute

20 ndash 40 times a minute

Pacemakers of the heart

1111

Cardiac Conduction

>

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

1111

Cardiac Conduction

>

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

Impulse Conduction amp the ECGSinoatrial node

AV nodeBundle of His

Bundle BranchesPurkinje fibers

The ldquoPQRSTrdquo

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

Normal Components of the EKG Waveform

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

ECG RULES

bull Professor Chamberlains 10 rules of normal-

1 PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

2 The width of the QRS complex should not exceed 110 ms less than 3 little squares

3 The QRS complex should be dominantly upright in leads I and II

4 QRS and T waves tend to have the same general direction in the limb leads

5 All waves are negative in lead aVR6 The R wave must grow from V1 to at least V4 The S

wave must grow from V1 to at least V3 and disappear in V6

7 The ST segment should start isoelectric8 The P waves should be upright in I II and V2 to V69 There should be no Q wave or only a small q less

than 004 seconds in width in I II V2 to V610 The T wave must be upright in I II V2 to V6

11

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

Normal tracing

R1

R2R3

R4

R5R6

R7

R8

R9NO ABNORMAL Q

R10

STANDARDISATION ECG amplitude scale

Normal amplitude

10 mmmV

Half amplitude

5 mmmV

Double amplitude

20 mmmV

Why ldquo1500 Xrdquo

bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute

bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10

OR

DR SHAFEI LASHEEN

Step 1 Calculate Rate when rhythm is regular

ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval

R wave

DRSHAFEI LASHEEN

HR if irregular rhythm

ndash Count the of R waves in a 6 second rhythm strip then multiply by 10

ndash Reminder all rhythm strips in the Modules are 6 seconds in length

Interpretation

9 x 10 = 90 bpm

3 sec 3 sec

DR SHAFEI LASHEEN

Step 2 Determine rhythm

bull Look at the R-R distances (using a caliper or markings on a pen or paper)

bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular

Interpretation Regular

R R

Regularity of Rhythm

DR SHAFEI LASHEEN

Axis

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Why ldquo1500 Xrdquo

bull Paper Speed 25 mm secbull 60 seconds minutebull 60 X 25 = 1500 mm minute bull 60 X 5 = 300 big square minute

bull Take 6 sec strip (30 large boxes)bull Count the PR waves X 10

OR

DR SHAFEI LASHEEN

Step 1 Calculate Rate when rhythm is regular

ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval

R wave

DRSHAFEI LASHEEN

HR if irregular rhythm

ndash Count the of R waves in a 6 second rhythm strip then multiply by 10

ndash Reminder all rhythm strips in the Modules are 6 seconds in length

Interpretation

9 x 10 = 90 bpm

3 sec 3 sec

DR SHAFEI LASHEEN

Step 2 Determine rhythm

bull Look at the R-R distances (using a caliper or markings on a pen or paper)

bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular

Interpretation Regular

R R

Regularity of Rhythm

DR SHAFEI LASHEEN

Axis

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Step 1 Calculate Rate when rhythm is regular

ndash Find a R wave that lands on a bold linendash Count the of large boxes to the next R wave ndash HR = 300 no large boxes between R-R intervalndash Count the of small boxes to the next R wavendash HR= 1500 no small boxes between R-R interval

R wave

DRSHAFEI LASHEEN

HR if irregular rhythm

ndash Count the of R waves in a 6 second rhythm strip then multiply by 10

ndash Reminder all rhythm strips in the Modules are 6 seconds in length

Interpretation

9 x 10 = 90 bpm

3 sec 3 sec

DR SHAFEI LASHEEN

Step 2 Determine rhythm

bull Look at the R-R distances (using a caliper or markings on a pen or paper)

bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular

Interpretation Regular

R R

Regularity of Rhythm

DR SHAFEI LASHEEN

Axis

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DRSHAFEI LASHEEN

HR if irregular rhythm

ndash Count the of R waves in a 6 second rhythm strip then multiply by 10

ndash Reminder all rhythm strips in the Modules are 6 seconds in length

Interpretation

9 x 10 = 90 bpm

3 sec 3 sec

DR SHAFEI LASHEEN

Step 2 Determine rhythm

bull Look at the R-R distances (using a caliper or markings on a pen or paper)

bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular

Interpretation Regular

R R

Regularity of Rhythm

DR SHAFEI LASHEEN

Axis

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Step 2 Determine rhythm

bull Look at the R-R distances (using a caliper or markings on a pen or paper)

bull Regular (are they equidistant apart) Occasionally irregular Regularly irregular Irregularly irregular

Interpretation Regular

R R

Regularity of Rhythm

DR SHAFEI LASHEEN

Axis

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Regularity of Rhythm

DR SHAFEI LASHEEN

Axis

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Axis

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

True LAD

bull So again if lead I is positive and aVF is negative we suspect LAD

bull To diagnose true LAD we examine lead IIndash If lead II is positive axis = 0deg to ndash30degndash If lead II is negative axis = ndash30deg to ndash90deg

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Extreme RAD

bull If lead I is negative AND aVF is also negative ndash extreme RAD

bull Clue If aVR is positive = extreme RADbull This is seen with rare situations such as VT or

Pacemakersbull In general we should never have an axis over

here

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Right axis deviation

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

P-waveNormal values1 up in all leads except

AVR2 Duration

lt 25 mm3 Amplitude lt 25 mm

Extreme RT axis

Abnormalities1 Inverted P-wavebull Junctional rhythm2 Wide P-wave (P- mitrale)bull LAE3 Peaked P-wave (P-pulmonale)bull RAE4 Saw-tooth appearancebull Atrial flutter5 Absent normal P wavebull Atrial fibrillation

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

P Pulmonale

P Mitrale

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Slide 9

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Slide 15

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Step 3 Assess the P waves

bull Are there P wavesbull Do the P waves all look alikebull Do the P waves occur at a regular ratebull Is there one P wave before each QRSInterpretation Normal P waves with 1 P

wave for every QRS

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

PR IntervalMeasured from the beginning of the P wave to the beginning of the Q waveNormal PR interval ranges from 012 to 020 second

PR interval

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

PR interval

Definition the time interval between beginning of P-wave to beginning of QRS complex

Normal PR interval 3-5mm or 3-5

small squares on ECG graph (012-02 sec)

Abnormalities 1 Short PR interval bull WPW syndrome2 Long PR interval bull First degree

heart block

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Slide 17

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Slide 44

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Step 4 Determine PR interval

bull Normal 012 - 020 seconds (3 - 5 boxes)

Interpretation 012 seconds

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

QRS Complex

Represents complete ventricular depolarization

QRS complex

QRS Complex Variants

QRS Complex

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

QRS complex

Normal valuesbull Duration lt 25 mmbull Morphology

progression from Short R and deep S (rs) in V1 to tall R and short S in V6 with small Q in V5-6

Abnormalities1 Wide QRS complex bull Bundle branch blockbull Ventricular rhythm

2 Tall R in V1bull RVHbull RBBBbull Posterior MIbull WPW syndrome 3 abnormal Q wave [ gt 25 of R wave]bull MIbull Hypertrophic

cardiomyopathybull Normal variant

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Small voltage QRS

bull Defined as lt 5 mm peak-to-peak in all limb leads or lt10 mm in precordial chest leads

bull causes mdash pulmonary disease hypothyroidism obesity cardiomyopathy

bull Acute causes mdash pleural andor pericardial effusions

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Step 5 QRS duration

bull Normal 004 - 012 seconds (1 - 3 boxes)

Interpretation 008 seconds

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Q Wave

Represents the beginning of septaldepolarization

The first negative deflection off of the baseline

Q Wave

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Q WAVES

bull Q waves lt004 secondbull Thatrsquos is less than one small square

durationbull Height lt25 or lt 14 of R wave height

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Normal Q wave

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

61

61

Normal Q waves

Notice the small Normal Q in Lead I

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Abnormal Q waves

bull The duration or width of Q waves becomes more than one small square on ECG graph

bull The depth of Q wave becomes more than 25 of R wave

bull The above changes comprise pathological Q wave and happens commonly in myocardial infarction and septal hypertrophy

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Q wave in MI

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

64

64Pathological Q wave

Notice the deep amp wide Infarction Q in Lead I

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Q wave in septal hypertrophy

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

R Wave

Indicates left ventricular depolarization

The first positive deflection off the baseline

R Wave

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Normal upward progression of R wave from V1 to V6

V1V2

V3V4

V5V6

The R wave in the precordial leads must grow from V1 to at least V4

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

T-waveNormal values1amplitude

lt 10mm in the chest leads

Abnormalities

1 Peaked T-wavebull Hyper-acute MIbull Hyperkalemiabull Normal variant

2 T- inversionbull Ischemiabull Myocardial infarctionbull Myocarditisbull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

NORMAL ST- SEGMENT

its isoelectric [ie at same level of PR or PQ segment at

least in the beginning]

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Abnormalities

1 ST elevationMore than one small squarebull Acute MIbull Prinzmetal anginabull Acute pericarditisbull Early repolarization

ST depressionMore than one small squarebull Ischemiabull Ventricular strainbull BBBbull Hypokalemiabull Digoxin effect

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Abnormalities of ST- segment

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Slide 11

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Slide 12

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

QT- interval

Definition Time interval between beginning of

QRS complex to the end of T waveNormally At normal HR QT le 11mm (044 sec) Abnormalities1 Prolonged QT interval hypocalcemia and

congenital long QT syndrome2 Short QT interval hypercalcemia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

QTc interval HR 70 QTlt 040 sec HR 80 QTlt 038 sec HR 60 QTlt 042 sec

lt 044 s gt 044 s

Normal Long QT

A prolonged QT can be very dangerous It may predispose an individual to a type of ventricular tachycardia called Torsades de Pointes Causes include drugs electrolyte abnormalities CNS disease post-MI and congenital heart disease

Torsades de Pointes

Long QT

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

EKG Intervals

1 P-wave lt 0110 sec (approximately 3 small boxes)

2 PR interval = beginning of the P-wave to the beginning of QRS Normal = 0120 ndash 0200 sec

3 QRS interval = from the first deflection to return to the baseline Normal lt 0120 sec

4 QT interval = beginning of the QRS to the END of the T-wave Normal lt 0450 sec

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

U WaveRepresents the last phase of

repolarizationThe exact significance is

unknownCharacteristic of

hypokalemiaMay predispose to

ventricular arrhythmias

U Wave

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Normal Sinus Rhythm

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

1 Every QRS is preceded by a P-wave

2 P-waves appear normal that is they are of sinus node origin

A Normal Morphology 1 P-wave duration lt 012 sec (lt 3 boxes) 2 P-wave height lt 25 mm

B Normal Axis ndash upright P-waves in lead II

Sinus Rhythmhellipor Not

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Rhythm Summary

bull Rate 90-95 bpmbull Regularity regularbull P waves normalbull PR interval 012 sbull QRS duration 008 sInterpretation Normal Sinus Rhythm

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

NSR Parameters

bull Rate 60 - 100 bpmbull Regularity regularbull P waves normalbull PR interval 012 - 020 sbull QRS duration 004 - 012 s

Any deviation from above is sinus Tachycardia sinus bradycardia or an arrhythmia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN 2010

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DREL SHAFEI A-AZIZ LASHEEN

Public Health Administration HAIL

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

What types of pathology can we identify and study from EKGs

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Arrhythmia Formation

Arrhythmias can arise from problems in thebull Sinus nodebull Atrial cellsbull AV junctionbull Ventricular cells

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

SA Node Problems

The SA Node canbull fire too slowbull fire too fast

SAN diseasesSinus Arrhythmia

Sinus BradycardiaSinus Tachycardia

(Sinus Tachycardia may be an appropriate response to stress)

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Rhythm 1

30 bpmbull Ratebull Regularity regular

normal

010 s

bull P wavesbull PR interval 012 sbull QRS duration

Interpretation Sinus Bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

DR SHAFEI LASHEEN

Rhythm 2

130 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 016 sbull QRS duration

Interpretation Sinus Tachycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Sinus block

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Missed cycle

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Sick Sinus Syndrome

Sinoatrial block (note the pauseis twice the P-P interval )

Sinus arrest with pause of 44 sbefore generation and conductionof a junctional escape beat

Severe sinus bradycardia

Sinus Arrhythmia

inspiration expiration

DR SHAFEI LASHEEN

Atrial Cell Problems

bull fire occasionally from a focus

bull fire continuously due to a looping re-entrant circuit

Premature Atrial Contractions (PACs)

Atrial Flutter

DR SHAFEI LASHEEN

Premature Atrial Contractions

bull Deviation from NSRndashThese ectopic beats originate in the atria

(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node

DR SHAFEI LASHEEN

Rhythm 3

70 bpmbull Ratebull Regularity occasionally irreg

27 different contour

008 s

bull P wavesbull PR interval 014 s (except 27)bull QRS duration

Interpretation NSR with Premature Atrial Contractions

Atrial Fibrillation

Atrial Fibrillation (A-fib)

DR SHAFEI LASHEEN

Rhythm 5

100 bpmbull Ratebull Regularity irregularly irregular

none

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Fibrillation

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

DR SHAFEI LASHEEN

Atrial Cell Problems

bull fire occasionally from a focus

bull fire continuously due to a looping re-entrant circuit

Premature Atrial Contractions (PACs)

Atrial Flutter

DR SHAFEI LASHEEN

Premature Atrial Contractions

bull Deviation from NSRndashThese ectopic beats originate in the atria

(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node

DR SHAFEI LASHEEN

Rhythm 3

70 bpmbull Ratebull Regularity occasionally irreg

27 different contour

008 s

bull P wavesbull PR interval 014 s (except 27)bull QRS duration

Interpretation NSR with Premature Atrial Contractions

Atrial Fibrillation

Atrial Fibrillation (A-fib)

DR SHAFEI LASHEEN

Rhythm 5

100 bpmbull Ratebull Regularity irregularly irregular

none

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Fibrillation

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

DR SHAFEI LASHEEN

Premature Atrial Contractions

bull Deviation from NSRndashThese ectopic beats originate in the atria

(but not in the SA node) therefore the contour of the P wave the PR interval and the timing are different than a normally generated pulse from the SA node

DR SHAFEI LASHEEN

Rhythm 3

70 bpmbull Ratebull Regularity occasionally irreg

27 different contour

008 s

bull P wavesbull PR interval 014 s (except 27)bull QRS duration

Interpretation NSR with Premature Atrial Contractions

Atrial Fibrillation

Atrial Fibrillation (A-fib)

DR SHAFEI LASHEEN

Rhythm 5

100 bpmbull Ratebull Regularity irregularly irregular

none

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Fibrillation

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

DR SHAFEI LASHEEN

Rhythm 3

70 bpmbull Ratebull Regularity occasionally irreg

27 different contour

008 s

bull P wavesbull PR interval 014 s (except 27)bull QRS duration

Interpretation NSR with Premature Atrial Contractions

Atrial Fibrillation

Atrial Fibrillation (A-fib)

DR SHAFEI LASHEEN

Rhythm 5

100 bpmbull Ratebull Regularity irregularly irregular

none

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Fibrillation

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

Atrial Fibrillation

Atrial Fibrillation (A-fib)

DR SHAFEI LASHEEN

Rhythm 5

100 bpmbull Ratebull Regularity irregularly irregular

none

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Fibrillation

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

Atrial Fibrillation (A-fib)

DR SHAFEI LASHEEN

Rhythm 5

100 bpmbull Ratebull Regularity irregularly irregular

none

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Fibrillation

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

DR SHAFEI LASHEEN

Rhythm 5

100 bpmbull Ratebull Regularity irregularly irregular

none

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Fibrillation

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

Atrial Flutter

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

DR SHAFEI LASHEEN

Rhythm 6

70 bpmbull Ratebull Regularity regular

flutter waves

006 s

bull P wavesbull PR interval nonebull QRS duration

Interpretation Atrial Flutter

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

DR SHAFEI LASHEEN

AV Junctional Problems

The AV junction canbull fire continuously

due to a looping re-entrant circuit

bull block impulses coming from the SA Node

Paroxysmal Supraventricular Tachycardia

AV Junctional Blocks

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

DR SHAFEI LASHEEN

Rhythm 7

74 148 bpmbull Ratebull Regularity Regular regular

Normal none

008 s

bull P wavesbull PR interval 016 s nonebull QRS duration

Interpretation Paroxysmal Supraventricular Tachycardia (PSVT)

AVNR tachycardia

AVNR tachycardia

Junctional Premature Beat

bull single ectopic beat that originates in the AV node or

bull Bundle of His area of the condunction systembull ndash Retrograde P waves immediately preceding the

QRS

bull ndash Retrograde P waves immediately following the QRS

bull ndash Absent P waves (buried in the QRS)

Premature Junctional Complexes (PJC)

Junctional Escape Beat

Junctional Rhythm

DR SHAFEI LASHEEN

Ventricular Cell Problems

Ventricular cells canbull fire occasionally

from 1 or more focibull fire continuously

from multiple focibull fire continuously

due to a looping re-entrant circuit

Premature Ventricular Contractions (PVCs)

Ventricular Fibrillation

Ventricular Tachycardia

DR SHAFEI LASHEEN

Ventricular Conduction

NormalSignal moves rapidly through the ventricles

AbnormalSignal moves slowly through the ventricles

Premature Ventricular Complex (PVC)

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Premature Junctional Complexes (PJC)

Junctional Escape Beat

Junctional Rhythm

DR SHAFEI LASHEEN

Ventricular Cell Problems

Ventricular cells canbull fire occasionally

from 1 or more focibull fire continuously

from multiple focibull fire continuously

due to a looping re-entrant circuit

Premature Ventricular Contractions (PVCs)

Ventricular Fibrillation

Ventricular Tachycardia

DR SHAFEI LASHEEN

Ventricular Conduction

NormalSignal moves rapidly through the ventricles

AbnormalSignal moves slowly through the ventricles

Premature Ventricular Complex (PVC)

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Junctional Escape Beat

Junctional Rhythm

DR SHAFEI LASHEEN

Ventricular Cell Problems

Ventricular cells canbull fire occasionally

from 1 or more focibull fire continuously

from multiple focibull fire continuously

due to a looping re-entrant circuit

Premature Ventricular Contractions (PVCs)

Ventricular Fibrillation

Ventricular Tachycardia

DR SHAFEI LASHEEN

Ventricular Conduction

NormalSignal moves rapidly through the ventricles

AbnormalSignal moves slowly through the ventricles

Premature Ventricular Complex (PVC)

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Junctional Rhythm

DR SHAFEI LASHEEN

Ventricular Cell Problems

Ventricular cells canbull fire occasionally

from 1 or more focibull fire continuously

from multiple focibull fire continuously

due to a looping re-entrant circuit

Premature Ventricular Contractions (PVCs)

Ventricular Fibrillation

Ventricular Tachycardia

DR SHAFEI LASHEEN

Ventricular Conduction

NormalSignal moves rapidly through the ventricles

AbnormalSignal moves slowly through the ventricles

Premature Ventricular Complex (PVC)

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Ventricular Cell Problems

Ventricular cells canbull fire occasionally

from 1 or more focibull fire continuously

from multiple focibull fire continuously

due to a looping re-entrant circuit

Premature Ventricular Contractions (PVCs)

Ventricular Fibrillation

Ventricular Tachycardia

DR SHAFEI LASHEEN

Ventricular Conduction

NormalSignal moves rapidly through the ventricles

AbnormalSignal moves slowly through the ventricles

Premature Ventricular Complex (PVC)

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Ventricular Conduction

NormalSignal moves rapidly through the ventricles

AbnormalSignal moves slowly through the ventricles

Premature Ventricular Complex (PVC)

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Premature Ventricular Complex (PVC)

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Rhythm 4

60 bpmbull Ratebull Regularity occasionally irreg

none for 7th QRS

008 s (7th wide)

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation Sinus Rhythm with 1 PVC

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

PVCs

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Ventricular Tachycardia (VT)

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

160 bpmbull Ratebull Regularity regular

none

wide (gt 012 sec)

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Tachycardia

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Ventricular Fibrillation (VF)

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Rhythm 9

nonebull Ratebull Regularity irregularly irreg

none

wide if recognizable

bull P wavesbull PR interval nonebull QRS duration

Interpretation Ventricular Fibrillation

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Torsade des points

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

AV Junctional Blocks

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

AV Blocks

AV Node Bundle of His

Right Bundle Branch Left Bundle Branch

Anterior Fascicle of Posterior Fascicle of

Left Bundle Left Bundle

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Classification of AV Heart Blocks

Degree AV Conduction Pattern

1St Degree Block Uniformly prolonged PR interval

2nd Degree Mobitz Type I Progressive PR interval prolongation

2nd Degree Mobitz Type II Sudden conduction failure

3rd Degree Block No AV conduction

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

60 bpmbull Ratebull Regularity regular

normal

008 s

bull P wavesbull PR interval 036 sbull QRS duration

Interpretation 1st Degree AV Block

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Second Degree AV Block

bull Mobitz type I or Winckebach

bull Mobitz type II

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Rhythm 11

50 bpmbull Ratebull Regularity regularly irregular

nl but 4th no QRS

008 s

bull P wavesbull PR interval lengthensbull QRS duration

Interpretation 2nd Degree AV Block Type I

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

nl 2 of 3 no QRS

008 s

bull P wavesbull PR interval 014 sbull QRS duration

Interpretation 2nd Degree AV Block Type II

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Third Degree AV Block(Complete Heart Block)

SA Node conducts at its AV Node conducts at its

inherent rate of 60-100 BPM inherent rate of 40-60 BPM

Two independent pacemakers

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Third Degree AV Block(Complete Heart Block)

P P P P P P P P P

QRS QRS QRS

Atria

AV Node

Ventricles

BLOCK

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

40 bpmbull Ratebull Regularity regular

no relation to QRS

wide (gt 012 s)

bull P wavesbull PR interval nonebull QRS duration

Interpretation 3rd Degree AV Block

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Acute Coronary Syndrome

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

ECG assessment

ST Elevation or new LBBBSTEMI

Non-specific ECGUnstable Angina

ST Depression or dynamicT wave inversions

NSTEMI

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

ECG Rhythm Interpretation

Acute Myocardial Infarction

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

ST Elevation and non-ST Elevation MIs

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

ECG Changes amp the Evolving MI

There are two distinct patterns of ECG change depending if the infarction is

ndashST Elevation (Transmural or Q-wave) orndashNon-ST Elevation (Subendocardial or non-Q-wave)

Non-ST Elevation

ST Elevation

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

ECG Changes

Ways the ECG can change include

Appearance of pathologic Q-waves

T-waves

peaked flattened inverted

ST elevation amp depression

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Sequence of changes in evolving AMI

1 minute after onset 1 hour or so after onset A few hours after onset

A day or so after onset Later changes A few months after AMI

Q

R

P

Q

TSTR

P

Q

ST

P

Q

T

ST

R

P

S

T

P

Q

TST

R

P

Q

T

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Views of the Heart

Some leads get a good view of the

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Anatomic Groups(Summary)

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Which part of the heart is affected

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

bull Leads V1 V2 V3 and V4 =

Anterior Wall MI

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Anterior infarctionAnterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left coronary Artery or LAD

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Anterior Wall MI

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

AWMI (pardeersquos sign)

The convex upwards ST elevation which is classical of acute myocardial infarction was described by Pardee in 1920 and has been called the ldquoPardeersquos signrdquo

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

ST Elevation (cont)

Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

What part of the heart is affected

I aVL V5 and V6 Lateral wall of left

ventricle

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Lateral infarctionLateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left circumflexcoronary artery

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Anterolateral MI

This personrsquos MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6 I and aVL)

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Infarct Is the ST elevation or depression

Yes Elevation in V2-V6 I and avL Depression in II III and avF

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

What part of the heart is affected II III aVF =

Inferior Wall

IIIIII

aVRaVLaVF

V1V2V3

V4V5V6

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

Inferior infarctionInferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right coronary artery

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

DR SHAFEI LASHEEN

Inferior Wall MI

This is an inferior MI Note the ST elevation in leads II III and aVF

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

177

177

Acute True Posterior MI

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

inferiorposterior STEMI with RV involvement

STEMI equivalent

Acute pericarditis

STEMI equivalent

Acute pericarditis

Acute pericarditis

Acute pulmonary embolism

45 yo female 1 week post-op with shortness of breath

Findings

bull Accelerated junctional rhythm

bull Right axis deviationbull ldquoS1Q3T3rdquo pattern

bull Clinical history and EKG most consistent with acute PE

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

ST depression amp T-wave inversion

The ECG changes seen with a non-ST elevation infarction are

Before injury Normal ECG

ST depression amp T-wave inversion

ST returns to baseline but T-wave inversion persists

Ischemia

Infarction

Fibrosis

ST Depression or Dynamic T wave Inversions

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

Herersquos an ECG of an evolving non-ST elevation MI

Note the ST depression and T-wave inversion in leads V2-V6

Question What area of the heart is infarcting

Anterolateral

Hypertrophy

DR SHAFEI LASHEEN

HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following

ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

Findings

bull Accelerated junctional rhythm

bull Right axis deviationbull ldquoS1Q3T3rdquo pattern

bull Clinical history and EKG most consistent with acute PE

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

ST depression amp T-wave inversion

The ECG changes seen with a non-ST elevation infarction are

Before injury Normal ECG

ST depression amp T-wave inversion

ST returns to baseline but T-wave inversion persists

Ischemia

Infarction

Fibrosis

ST Depression or Dynamic T wave Inversions

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

Herersquos an ECG of an evolving non-ST elevation MI

Note the ST depression and T-wave inversion in leads V2-V6

Question What area of the heart is infarcting

Anterolateral

Hypertrophy

DR SHAFEI LASHEEN

HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following

ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

ST depression amp T-wave inversion

The ECG changes seen with a non-ST elevation infarction are

Before injury Normal ECG

ST depression amp T-wave inversion

ST returns to baseline but T-wave inversion persists

Ischemia

Infarction

Fibrosis

ST Depression or Dynamic T wave Inversions

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

Herersquos an ECG of an evolving non-ST elevation MI

Note the ST depression and T-wave inversion in leads V2-V6

Question What area of the heart is infarcting

Anterolateral

Hypertrophy

DR SHAFEI LASHEEN

HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following

ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

ST Depression or Dynamic T wave Inversions

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

Herersquos an ECG of an evolving non-ST elevation MI

Note the ST depression and T-wave inversion in leads V2-V6

Question What area of the heart is infarcting

Anterolateral

Hypertrophy

DR SHAFEI LASHEEN

HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following

ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

Non-ST Elevation Infarction

Herersquos an ECG of an evolving non-ST elevation MI

Note the ST depression and T-wave inversion in leads V2-V6

Question What area of the heart is infarcting

Anterolateral

Hypertrophy

DR SHAFEI LASHEEN

HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following

ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

Hypertrophy

DR SHAFEI LASHEEN

HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following

ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

HypertrophyIn this step of the 12-lead ECG analysis we use the ECG to determine if any of the 4 chambers of the heart are enlarged or hypertrophied We want to determine if there are any of the following

ndash Right atrial enlargement (RAE)ndash Left atrial enlargement (LAE)ndash Right ventricular hypertrophy (RVH)ndash Left ventricular hypertrophy (LVH)

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

Slide 15

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

ndash To diagnose RAE you can use the following criteriabull II P gt 25 mm orbull V1 or V2 P gt 15 mm

Right atrial enlargement

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

Left atrial enlargement ndash To diagnose LAE you can use the following criteria

bull II gt 004 s (1 box) between notched peaks orbull V1 Neg deflection gt 1 box wide x 1 box deep

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

199

199

Ventricular Hypertrophybull Ventricular Muscle

Hypertrophybull QRS voltages in V1 and V6 L

1 and aVLbull We may have to record to frac12

standardizationbull T wave changes opposite to

QRS directionbull Associated Axis shiftsbull Associated Atrial hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

Left Ventricular Hypertrophy

Why is left ventricular hypertrophy characterized by tall QRS complexes

LVH ECHOcardiogramIncreased QRS voltage

As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

Criteria for LVH

bull Sokolow-Lyonndash S v1+R v5v6gt35mm

ndash R I+S IIIgt25mmndash R avlgt11mm

bull Cornellndash S v3+R avl gt28 (men)

gt20( women)

bull Romhilt-Estesndash LV strain

3ndash LAE 3ndash LAD 2ndash QRS duration 1

ndash R v5v6gt3 3

ndash Sv1v2gt33

ndash Largest R or Sgt2 3

5 or more points suggests LVH

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

203

203Left Ventricular Hypertrophy

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

LV+LA

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

205

205Right Ventricular Hypertrophy

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

Bundle Branch Blocks

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DR SHAFEI LASHEEN

Right Bundle Branch BlocksWhat QRS morphology is characteristic

For RBBB the wide QRS complex assumes a unique virtually diagnostic shape in those leads overlying the right ventricle (V1 and V2)

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

209

209Complete RBBB

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

DRSHAFEI LASHEEN

Left Bundle Branch BlocksWhat QRS morphology is characteristicFor LBBB the wide QRS complex assumes a characteristic change in shape in those leads opposite the left ventricle (right ventricular leads - V1 and V2)

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

211

211Complete LBBB

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

Miscellaneous

K Ca

Hyperkalaemia

K=94 mmoll

K Ca

Hyperkalaemia

K=94 mmoll

Hyperkalaemia

K=94 mmoll

K=94 mmoll

Hypokalaemia

K= 15

K= 15

Hypocalcaemia

Pericardial Effusion (electrical alternans)

Hypothermia (osborne wave)

Pericardial Effusion (electrical alternans)

Hypothermia (osborne wave)

Hypothermia (osborne wave)

Arrythmogenic RV dysplasia(Epsilon wave)

Digitalis toxicity

SAH(t wave +long QT)

SAH(t wave +long QT)

WPW syndrome

WPW + AF

Ventricular Pacemaker (Single Chamber)

pacemaker

Dual Paced Rhythmpacemaker

AV pacing

WPW + AF

Ventricular Pacemaker (Single Chamber)

pacemaker

Dual Paced Rhythmpacemaker

AV pacing

Ventricular Pacemaker (Single Chamber)

pacemaker

Dual Paced Rhythmpacemaker

AV pacing

Dual Paced Rhythmpacemaker

AV pacing

AV pacing

Cable reversal

Dextrocardia

Artifacts in Parkinsonrsquos pt

Artifacts in Parkinsonrsquos pt

Movements Artifacts

Electric noise

DR SHAFEI LASHEEN 2010

Thank You

DR SHAFEI LASHEEN 2015

• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Horizontal plane - the six chest leads
• The 12-Leads
• Slide 10
• Cardiac Conduction
• Impulse Conduction amp the ECG
• Slide 13
• Slide 14
• Slide 15
• ECG RULES
• Slide 17
• Slide 18
• STANDARDISATION ECG amplitude scale
• Slide 20
• Why ldquo1500 Xrdquo
• Slide 22
• Slide 23
• Slide 24
• Regularity of Rhythm
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Slide 32
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• P-wave
• P Pulmonale
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• PR Interval
• PR interval
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• QRS Complex
• QRS complex
• Small voltage QRS
• Slide 55
• Slide 56
• Slide 57
• Q Wave
• Q WAVES
• Normal Q wave
• Normal Q waves
• Abnormal Q waves
• Q wave in MI
• Pathological Q wave
• Q wave in septal hypertrophy
• Slide 66
• R Wave
• Normal upward progression of R wave from V1 to V6
• Slide 69
• Slide 70
• T-wave
• Slide 72
• NORMAL ST- SEGMENT
• Abnormalities
• Abnormalities of ST- segment
• Slide 76
• Slide 77
• Slide 78
• QT- interval
• Slide 80
• Slide 81
• Slide 82
• U Wave
• Slide 84
• Slide 85
• Slide 86
• Slide 87
• Slide 88
• (2)
• Slide 90
• Slide 91
• Slide 92
• Slide 93
• Slide 94
• Sinus block
• Slide 96
• Sick Sinus Syndrome
• Sinus Arrhythmia
• Slide 99
• Slide 100
• Slide 101
• Slide 102
• Atrial Fibrillation
• Atrial Fibrillation (A-fib)
• Slide 105
• Slide 106
• Atrial Flutter
• Slide 108
• Slide 109
• Slide 110
• AVNR tachycardia
• Junctional Premature Beat
• Premature Junctional Complexes (PJC)
• Junctional Escape Beat
• Junctional Rhythm
• Slide 116
• Slide 117
• Premature Ventricular Complex (PVC)
• Slide 119
• Slide 120
• Slide 121
• Slide 122
• Slide 123
• Slide 124
• Ventricular Tachycardia (VT)
• Slide 126
• Ventricular Fibrillation (VF)
• Slide 128
• Torsade des points
• Slide 130
• Slide 131
• Slide 132
• AV Junctional Blocks
• AV Blocks
• Slide 135
• Classification of AV Heart Blocks
• Slide 137
• Second Degree AV Block
• Slide 139
• Slide 140
• Third Degree AV Block (Complete Heart Block)
• Third Degree AV Block (Complete Heart Block)
• Slide 143
• Slide 144
• Acute Coronary Syndrome
• Slide 146
• Slide 147
• Slide 148
• Slide 149
• Slide 150
• Slide 151
• Slide 152
• Slide 153
• Sequence of changes in evolving AMI
• Slide 155
• Slide 156
• Slide 157
• Slide 158
• Slide 159
• Slide 160
• Slide 161
• Slide 162
• Slide 163
• Slide 164
• Anterior infarction
• Slide 166
• AWMI (pardeersquos sign)
• Slide 168
• Slide 169
• Lateral infarction
• Slide 171
• Slide 172
• Slide 173
• Slide 174
• Inferior infarction
• Slide 176
• Acute True Posterior MI
• Slide 178
• Slide 179
• Slide 180
• Slide 181
• Slide 182
• Acute pericarditis
• Acute pulmonary embolism
• Slide 185
• Findings
• Slide 187
• Slide 188
• Slide 189
• Slide 190
• Slide 191
• Hypertrophy
• Slide 193
• Slide 194
• Slide 195
• Slide 196
• Slide 197
• Slide 198
• Ventricular Hypertrophy
• Slide 200
• Slide 201
• Criteria for LVH
• Left Ventricular Hypertrophy
• LV+LA
• Right Ventricular Hypertrophy
• Slide 206
• Slide 207
• Slide 208
• Complete RBBB
• Slide 210
• Complete LBBB
• Slide 212
• Slide 213
• Slide 214
• Miscellaneous
• Slide 216
• Slide 217
• Slide 218
• Slide 219
• Slide 220
• Hyperkalaemia
• K=94 mmoll
• Hypokalaemia
• K= 15
• Slide 225
• Pericardial Effusion (electrical alternans)
• Hypothermia (osborne wave)
• Slide 228
• Arrythmogenic RV dysplasia (Epsilon wave)
• Digitalis toxicity
• SAH(t wave +long QT)
• Slide 232
• WPW + AF
• Ventricular Pacemaker (Single Chamber)
• Slide 235
• Dual Paced Rhythm
• AV pacing
• Cable reversal
• Slide 239
• Dextrocardia
• Artifacts in Parkinsonrsquos pt
• Movements Artifacts
• Slide 243
• Slide 244
• Electric noise
• Slide 246