1. ADVANCED EKG INTERPRETATION
Edward Briggs DNP

2. 12 LEAD EKG INTERPRETATION
Objectives
Review basic EKG components
Discuss the process of interpreting an EKG
Discuss Axis interpretation and clinical significance
Discuss EKG changes indicative of:
Ischemia (acute and resolving)
Myocardial scar/old MI
Hypertrophy/Strain
Pericarditis
Other (i.e. electrolytes and EKG changes, medication effects)

3. KEY POINTS
Establish a process and follow it each time you interpret an EKG
Don’t skip steps
Never trust the EKG interpretation and always confirm the interpretation yourself
If unsure of the interpretation consult

4. KEY POINTS Make sure it is a good tracing
If difficult to read it have it repeated
If old EKG is available always compare to the old EKG
Remember to treat the clinical presentation and not the EKG. Myocardial Infarction may not demonstrate EKG changes initially, especially in small or multi - vessel disease

5. 12 Lead EKG Interpretation
Follow the process
Determine rate (normal, tachy, brady)
Regularity (regular, irregular)
Intervals (PR interval, QRS duration, QTc)
Define underlying rhythm (sinus rhythm, atrial fib, 1st degree block, etc.)

6. 12 Lead EKG Interpretation
Follow the process
5. Determine Axis (Normal, RAD, LAD, indeterminate)
6. Evaluate waveform morphology
P wave (Peaked, notched – suggestive of atrial/pulmonary disease process)
QRS height (LVH), BBB, pacer spikes, widening
T wave slurring, peaked (hyperkalemia)

7. 12 Lead EKG Interpretation
Follow the process
7. Evaluate ST segments
Evaluate all ST’s
Consider ST changes corresponding to region (II, III, AVF = inferior wall, etc)
Note the deflection and shape of any ST changes
Depression, elevation, concave, convex
8. Evaluate for Q Waves

8. Quick Review The various intervals seen on the EKG include:
The P wave: represents atrial depolarization
PR Interval
(measured from beginning of P to beginning of QRS in the frontal plane)
•Normal: s
•Short PR: < 0.12s ◦Preexcitation syndromes: WPW (Wolff-Parkinson-White) Syndrome: An accessory pathway (called the "Kent" bundle) connects the right atrium to the right ventricle or the left atrium to the left ventricle, and this permits early activation of the ventricles (delta wave) and a short PR interval.
image 01-02
LGL (Lown-Ganong-Levine): An AV nodal bypass track into the His bundle exists, and this permits early activation of the ventricles without a delta-wave because the ventricular activation sequence is normal.
•Prolonged PR: > 0.20s ◦First degree AV block (PR interval usually constant) ◾Intra-atrial conduction delay (uncommon)
Slowed conduction in AV node (most common site)
Slowed conduction in His bundle (rare)
Slowed conduction in bundle branch (when contralateral bundle is blocked)
◦Second degree AV block (PR interval may be normal or prolonged; some P waves do not conduct) ◾Type I (Wenckebach): Increasing PR until nonconducted P wave occurs
Type II (Mobitz): Fixed PR intervals plus nonconducted P waves
◦ AV dissociation: Some PR's may appear prolonged, but the P waves and QRS complexes are dissociated (i.e., not married, but strangers passing in the night).
Norm ms
Short PR <0.12 ms
= Wolf Parkinson White
Pr > 0.2 = 1ST or 2nd Degree AVB

9. Quick Review The various intervals seen on the EKG include:
The P wave: represents atrial depolarization
The QRS complex: represents ventricular depolarization
The ST segment: represents the total ventricular repolarization time
The T wave: represents the rapid phase of ventricular repolarization
The QT interval: represents the entirety of ventricular systole
QRS Duration
0.06 – 0.12 ms
QRS >0.12 ms
=BBB or IVCD
QRS Duration
(duration of QRS complex in frontal plane):
•Normal: s
•Prolonged QRS Duration (> 0.10s): ◦QRS duration s ◾Incomplete right or left bundle branch block
Nonspecific intraventricular conduction delay (IVCD)
Some cases of left anterior or posterior fascicular block
◦QRS duration ≥ 0.12s ◾Complete RBBB or LBBB
◾Nonspecific IVCD
◾Ectopic rhythms originating in the ventricles (e.g., ventricular tachycardia, pacemaker rhythm)
Norm ms
Short PR <0.12 ms
= Wolf Parkinson White
Pr > 0.2 = 1ST or 2nd Degree AVB

10. Quick Review The various intervals seen on the EKG include:
The P wave: represents atrial depolarization
The QRS complex: represents ventricular depolarization
The T wave: represents the rapid phase of ventricular repolarization
The QT interval: represents the entirety of ventricular systole
QRS Duration
0.06 – 0.12 ms
QRS >0.12 ms
=BBB or IVCD
QT Interval
(measured from beginning of QRS to end of T wave in the frontal plane)
•Normal: heart rate dependent (corrected QT = QTc = measured QT, sq-root RR in seconds; upper limit for QTc = 0.44 sec)
• Long QT Syndrome - "LQTS" (based on upper limits for heart rate; QTc ≥ 0.47 sec for males and ≥ 0.48 sec in females is diagnostic for hereditary LQTS in absence of other causes of increased QT) ◦ This abnormality may have important clinical implications since it usually indicates a state of increased vulnerability to malignant ventricular arrhythmias, syncope, and sudden death. The prototype arrhythmia of the Long QT Interval Syndromes (LQTS) is Torsade-de-pointes, a polymorphic ventricular tachycardia characterized by varying QRS morphology and amplitude around the isoelectric baseline. Causes of LQTS include the following: ◾Drugs (many antiarrhythmics, tricyclics, phenothiazines, and others)
◾Electrolyte abnormalities (↓K+, ↓Ca++, ↓Mg++)
◾CNS disease (especially subarrachnoid hemorrhage, stroke, trauma)
◾Hereditary LQTS (e.g., Romano-Ward Syndrome)
◾Coronary Heart Disease (some post-MI patients)
Norm ms
QT Interval
Rate dependent
Normal Rate <0.44ms
Short PR <0.12 ms
= Wolf Parkinson White
Pr > 0.2 = 1ST or 2nd Degree AVB

11. Quick Review
The baseline of the EKG is defined as the isoelectric or flat line seen between the waveforms that comprise the P wave, QRS complex, and T wave.
When considering segment elevation or depression, each small box represents 1 mm. You will hear ST segment elevation or depression described by the number of millimeters it is above or below the baseline.
Isoelectric
line

12. Quick Review
The ST segment is the flat area of baseline situated between the QRS complex and T wave that represents the initial phase of ventricular repolarization, referred to as the plateau phase

13. Quick Review - Rate
The classic 12-lead EKG represents about 6 seconds of time. On the EKG paper, one large box is equal to 200 milliseconds or 0.2 seconds. Each large box is composed of five smaller boxes, each equal to 40 milliseconds or 0.04 seconds. This is helpful to remember when estimating intervals
0.04 seconds
0.2 seconds
Rate can be measured by counting QRS occurrence in 6 seconds and multiply by ten, or by counting number of large boxes between QRSs, if regular (300,150,100,75,60,50)

14. RATE Quick and easy way to “guess” rate:
IF regular rhythm count the number of large boxes between QRS
If one large box between QRS then rate = 300 BPM
If two large boxes between QRS then rate = 150
If three large boxes between QRS then rate = 75
Etc.
If irregular rhythm count the number of QRS complexes documented on the EKG in the rhythm strip and multiply by 10

15. REGULARITY
QUICK AND EASY WAY TO DETERMINE REGULARITY IS TO MEASURE ONE
QRS COMPLEX TO THE NEXT. THEN EVALUATE IS THIS IS CONSISTENT THROUGHOUT
THE EKG.

16. Quick Review The various intervals seen on the EKG include:
The P wave: represents atrial depolarization
The QRS complex: represents ventricular depolarization
The ST segment: represents the total ventricular repolarization time
The T wave: represents the rapid phase of ventricular repolarization
The QT interval: represents the entirety of ventricular systole
QRS Duration
0.06 – 0.12 ms
QT Interval
(measured from beginning of QRS to end of T wave in the frontal plane)
•Normal: heart rate dependent (corrected QT = QTc = measured QT, sq-root RR in seconds; upper limit for QTc = 0.44 sec)
• Long QT Syndrome - "LQTS" (based on upper limits for heart rate; QTc ≥ 0.47 sec for males and ≥ 0.48 sec in females is diagnostic for hereditary LQTS in absence of other causes of increased QT) ◦ This abnormality may have important clinical implications since it usually indicates a state of increased vulnerability to malignant ventricular arrhythmias, syncope, and sudden death. The prototype arrhythmia of the Long QT Interval Syndromes (LQTS) is Torsade-de-pointes, a polymorphic ventricular tachycardia characterized by varying QRS morphology and amplitude around the isoelectric baseline. Causes of LQTS include the following: ◾Drugs (many antiarrhythmics, tricyclics, phenothiazines, and others)
◾Electrolyte abnormalities (↓K+, ↓Ca++, ↓Mg++)
◾CNS disease (especially subarrachnoid hemorrhage, stroke, trauma)
◾Hereditary LQTS (e.g., Romano-Ward Syndrome)
◾Coronary Heart Disease (some post-MI patients)
Norm ms
QT Interval
Rate dependent
Normal Rate <0.44ms

17. RHYTHM Determine the underlying rhythm Normal Sinus Rhythm
Sinus Arrhythmia
Atrial Fibrillation
Ectopic Beats
Etc.
Whenever you detect a variance from the “norm” i.e. blocks, a-fib, etc. determine if this is a new phenomenon or chronic. If new then need to determine why.

18. 12 Lead EKG
Review and discussion

19. 12 Lead EKG
Each of these leads records the same electrical activity, but from a different angle.
This is why the EKG tracing will vary from lead to lead.
As depolarization spreads toward a positive pole, there is an upward deflection in that lead.
As it spreads away from a positive pole, there is a downward deflection in that lead. Take the vantage point of each positive pole. As electricity moves toward it, the respective EKG deflection appears positive. As electricity moves away from it, it appears negative

20. EKG CHANGES
An analogy
Think of the electrical flow across the myocardium as a river
If you look at the river from different banks it looks different, but the river hasn’t changed
Now imagine a beaver builds a dam along that river, we see actual change in the flow of the river
The “dam” would be ischemia/scar that would be changing the course of the myocardial electrical flow

21. 12 lead EKG Made up of Bipolar leads : I, II, III
Lead I records the electrical difference between the left arm and the right arm electrodes and is positive on the left and negative on the right
Lead II records the electrical difference between the left leg and the right arm electrodes and is positive at the leg and negative at the arm
Lead III records the electrical difference between the left leg and the left arm electrodes and is positive at the leg and negative at the arm

22. 12 lead EKG Unipolar Augmented Leads – aVR, aVF, and aVL
aVR: Augmented voltage right arm: a combination of leads I and II
aVL: Augmented voltage left arm: a combination of leads I and III
aVF: Augmented voltage foot: a combination of leads II and III

23. 12 Lead EKG
Precordial Leads: V1 V2 V3 V4 V5 V6

24. 12 Lead EKG
Combinations of leads represent flow of electricity as moves over different aspects of the heart
These 12 leads should be always considered in groups because each set of leads represents a specific area of the myocardium
Leads I, aVL, V5, and V6 are the lateral leads.
Leads II, III, and aVF are the inferior leads.
Leads V1 to V4 are the anterior chest leads.
Leads V1, V2 are the anterior septal leads

25. 12 Lead EKG
Each myocardium region is perfused by specific coronary arteries, therefore each cardiac region has corresponding coronary arteries
Anterior
AnterioSeptal
Inferior
Lateral

26. Determine Axis
Axis = electrically where the heart lies in the chest

27. Axis
Axis refers to the general direction of electrical conduction through the heart.
It gives a graphical representation of the electrical position of the heart
Deviation from “normal” represents either malposition of the heart itself or;
Something is altering how the electricity flows over the heart (ischemia, scar, blocks, etc.)

28. AXIS Axis deviations are divided into 2 categories:
Right Axis Deviation (RAD)
Left Axis Deviation (LAD)
Deviations can occur from physiologic conditions such as obesity, physical morphology (tall thin stretching out myocardium, cavitus pectorum physically rotating the heart)
Deviations can occur from pathologic conditions such as ischemia, infarct altering the electrical flow

29. Determining Axis Normal axis : 0 to -90 degrees
RAD : + 90 to +/- 180 degrees
LAD : 0 to -90 degrees
Indeterminate : -90 to +/- 180

30. Determining Axis Easy Trick: Hold up your left thumb and right thumb
Left thumb corresponds to lead I
Right thumb corresponds to lead AVF
If lead I is upright and aVF is upright axis is normal
If lead I is upright and aVF is downward axis is left (LAD)
If lead I is downward and aVF is upright axis is right (RAD)
If Lead I and AVF are downward Northwest Region (No Man’s Land)

31. LEFT AXIS DEVIATION (LAD)
AXIS DEVIATIONS
LEFT AXIS DEVIATION (LAD)
Lateral wall myocardial infarction
Left ventricular hypertrophy
Left bundle branch block
Left anterior fascicular block

32. AXIS DEVIATIONS RIGHT AXIS DEVIATION (RAD)
Left posterior fascicular block
Right bundle branch block
Right ventricular hypertrophy
Obesity Tall, thin frame, cavitus pectorum
Inferior wall myocardial infarction
COPD

33. AXIS DEVIATIONS
NO MAN’S LAND (NORTHWEST REGION) •emphysema/copd •hyperkalaemia •lead transposition •artificial cardiac pacing •ventricular tachycardia

34. Wave Form Morphology P-Wave
Represents Depolarization across the Atria
Normal – 1 P wave precedes each QRS
Rounded hump
Normal PR interval is < 0.20 ms

35. Wave Form Morphology P-Wave

36. Wave Form Morphology P-Wave
The principal cause is pulmonary hypertension due to:
•Chronic lung disease (cor pulmonale)
•Tricuspid stenosis
•Congenital heart disease (pulmonary stenosis, Tetralogy of Fallot)
•Primary pulmonary hypertension

37. Wave Form Morphology P-Wave
P mitrale
The presence of broad, notched (bifid) P waves in lead II is a sign of left atrial enlargement, classically due to:
mitral stenosis.

38. Wave Form Morphology QRS Complex
Represents depolarization of the left and right ventricle
Look to the QRS complexes in the precordial leads (V1-V6)
Evaluate R wave progress
Evaluate height and width of the QRS complexes

39. Hypertrophy
Hypertrophy is thickening of the heart muscle secondary to some strain
Think of increased workload (Body builders muscles become hypertrophic in response to increase workload)
CLUE:
Right side think pulmonary
Left side think systemic

40. Poor R Wave Progression
Definition
R wave height ≤ 3 mm in V3.
Causes
Prior anteroseptal MI
Left ventricular hypertrophy
Inaccurate lead placement (e.g. transposition of V1 and V3)
Dilated cardiomyopathy
May be a normal variant

41. Wave Form Morphology QRS Complex – Left Ventricular Hypertrophy
-QRS complex is slightly widened (about 0.11 sec), -Left Axis Deviation
-Tall R waves are present in multiple leads, and
-ST-T changes (formerly called a "strain" pattern) are present.
-Frequent concurrent P wave abnormalities
Left ventricular hypertrophy (LVH) refers to an increase in the size of myocardial fibers in the main cardiac pumping chamber. Such hypertrophy is usually the response to a chronic volume or pressure load.
●The two most important pressure overload states are systemic hypertension and aortic stenosis
●The major conditions associated with left ventricular volume overload are aortic or mitral valve regurgitation and dilated cardiomyopathy.

42. Wave Form Morphology QRS Complex – Right Ventricular Hypertrophy
Clues to the diagnosis include:
●Right axis deviation (>+90)
●R in V1 >6 mm
●R/S ratio in V1 >1
●Incomplete right bundle branch block
●ST-T wave abnormalities ("strain") in inferior leads
●Right atrial hypertrophy/overload (“P pulmonale”)
●S>R in leads I, II, III, particularly in children (S1S2S3 pattern)
Right ventricular hypertrophy (RVH) is present when there is a pathologic increase in muscle mass of the right ventricle.
Commonly seen with pulmonary hypertension, pulmonic stenosis, or severe lung disease and cor pulmonale.

43. ABNORMAL EKG - blocks RIGHT BUNDLE BRANCH BLOCK
In RBBB, activation of the right ventricle is delayed as depolarization has to spread across the septum from the left ventricle.
The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged.
The delayed right ventricular activation produces a secondary R wave (R’) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads.
Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads.
In isolated RBBB the cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch.

44. ABNORMAL EKG - blocks RIGHT BUNDLE BRANCH BLOCK Causes of RBBB
Right ventricular hypertrophy / cor pulmonale
Pulmonary embolus
Ischemic heart disease
Rheumatic heart disease
Myocarditis or cardiomyopathy
Degenerative disease of the conduction system
Congenital heart disease (e.g. atrial septal defect)

45. ABNORMAL EKG - blocks RIGHT BUNDLE BRANCH BLOCK Diagnostic Criteria
•Broad QRS > 120 ms
•RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
•Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
QRS >120ms
Slurred S
Wave

46. ABNORMAL EKG - blocks LEFT BUNDLE BRANCH BLOCK
Normally the septum is activated from left to right, producing small Q waves in the lateral leads.
In LBBB, septal depolarization is reversed (becomes right to left), as the impulse spreads first to the RV via the right bundle branch and then to the LV via the septum.
This sequence of activation extends the QRS duration to > 120 ms and eliminates the normal septal Q waves in the lateral leads.
The overall direction of depolarization (from right to left) produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3), and usually leads to left axis deviation.
As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched (‘M’-shaped) R wave in the lateral leads.

47. ABNORMAL EKG - blocks LEFT BUNDLE BRANCH BLOCK Causes Aortic stenosis
Ischemic heart disease
Hypertension
Dilated cardiomyopathy
Anterior MI
Primary degenerative disease (fibrosis) of the conducting system (Lenegre disease)
Hyperkalemia
Digoxin toxicity

48. ABNORMAL EKG - Blocks LEFT BUNDLE BRANCH BLOCK Diagnostic Criteria
•QRS duration of > 120 ms
•Dominant S wave in V1
•Broad monophasic R wave in lateral leads (I, aVL, V5-V6)
•Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL)
•Prolonged R wave peak time > 60ms in left precordial leads (V5-6)
QRS >120ms
Monophasic R waves
Dominant S

49. EXAMPLES Interpretation : SINUS TACH WITH BBB LEFT
QRS >120ms
‘W’ V1
‘M’ V6
Interpretation :
Rate – Regularity – Regular
Intervals
PR – 0.16
QRS – 160 ms
QT – 350ms
AXIS – Left Axis Deviation
SINUS TACH WITH BBB
LEFT
“W” in V1
“M” in V6

50. EXAMPLES Interpretation : Rate – 78 Regularity – Regular
QRS >120ms
‘M’ V1
‘W’ V6
Interpretation :
Rate – Regularity – Regular
Intervals
PR – 0.16
QRS – 160 ms
QT – 340ms
AXIS – normal
SINUS TACH WITH BBB
RIGHT
“M” in V1
“W” in V6

51. ABNORMAL EKG - blocks INTRAVENTRICULAR CONDUCTION DELAY
Definition : Conduction of impulse is delayed as it moves through the ventricle
QRS duration > 100 ms in the presence of a supraventricular rhythm.
Most commonly due to bundle branch block or left ventricular hypertrophy.
The most important life-threatening causes of QRS widening are hyperkaliemia and tricyclic antidepressant poisoning.
New Onset block? Think electrolytes and overdose!

52. ABNORMAL EKG - blocks INTRAVENTRICULAR CONDUCTION DELAY Types
Left anterior fascicular block
Left posterior fascicular block
Left bundle branch block
Right bundle branch block
Bifascicular block
Trifascicular block

53. ABNORMAL EKG - blocks Types •Left anterior fascicular block
INTRAVENTRICULAR CONDUCTION DELAY
Types
•Left anterior fascicular block
In left anterior fascicular block (aka left anterior hemiblock), impulses are conducted to the left ventricle via the left posterior fascicle, which inserts into the infero-septal wall of the left ventricle along its endocardial surface.

54. ABNORMAL EKG - blocks Types INTRAVENTRICULAR CONDUCTION DELAY
In left posterior fascicular block
(aka left posterior hemiblock), impulses are conducted to the left ventricle via the left anterior fascicle, which inserts into the upper, lateral wall of the left ventricle along its endocardial surface.

55. ABNORMAL EKG - blocks Types INTRAVENTRICULAR CONDUCTION DELAY
•Bifascicular block is the combination of RBBB with either LAFB or LPFB.
Trifascicular block (TFB) refers to the presence of conducting disease in all three fascicles:
Right bundle branch (RBB)
Left anterior fascicle (LAF)
Left posterior fascicle (LPF)

56. Electrolyte effects

57. Electrolyte effects HYPERCALCEMIA HYPOCALCEMIA T wave
Broad tall Peaked
P wave
Flattening/absent
QRS
Widening
narrow
ST Segment
Prolonged, depressed QT
shortened
Prolonged
U wave
Ectopy
Uncommon
J-waves
Torsades De Pointes

58. Electrolyte effects HYPERKALEMIA HYPOKALEMIA T wave Peaked Negative
P wave
Flattening
QRS
Widening
ST Segment
Depression/flatten QT
Prolonged
U wave
Present
Ectopy
Ventricular ectopy
Atrial Fib/Flutter
Vent fib

59. Medication Effects on ECG
The most common drugs ingested that may show QRS and/or QT prolongation and arrhythmias (though these are not always present) are: •Calcium channel blockers (particularly verapamil and diltiazem) •Beta blockers (particularly propranolol and sotalol ) •Digoxin •Tricyclic antidepressants •Antipsychotic drugs (particularly thioridazine) •Anticonvulsants (particularly carbamazepine and phenytoin) •Dextropropoxyphene •Antimalarial drugs (chloroquine, quinine) •Antiarrhythmic drugs •Orphenadrine •Lithium (cation)

60. ST Segment
When examining the ST segment, be careful to look for the presence of ST segment elevation or depression. The ST segment should be isoelectric or flat on the baseline. Clinical Point : Deviation of 2 mm (two small boxes) above or below the baseline is indicative of a pathologic process.

61. Critical analysis for acute ischemic events
ST SEGMENT
Critical analysis for acute ischemic events

62. ST Segment
The T wave is usually concordant with the QRS complex. Thus if the QRS complex is positive in a certain lead than the T wave usually is positive too in that lead.
Accordingly the T wave is normally upright or positive in leads I, II, AVL, AVF and V3-V6. The T wave is negative in V1 and AVR. The T wave flips around V2, but there is likely some genetic influence in this as in Blacks the T wave usually flips around V3.
The T wave angle is the result of small differences in the duration of the repolarization between the endocardial and epicardial layers of the left ventricle.

63. ST Segment elevation
ELEVATION OF THE ST SEGMENT OF THE ECG CAN RESULT FROM MULTIPLE PATHOLOGIES, INCLUDING:
LVH, LBBB, Pericarditis, Hyperkalemia, Anterior AMI.
Acute pericarditis: ST elevation in all leads except aVR
Pulmonary embolism: ST elevation in V1 and aVR
Hypothermia: ST elevation in V3-V6, II, III and aVF
Hypertrophic cardiomyopathy: V3-V5 (sometimes V6)
High potassium (hyperkalemia): V1-V2 (V3)
During acute neurologic events: all leads, primarily V1-V6
Acute sympathic stress: all leads, especially V1-V6
Brugada syndrome.**
Cardiac aneurysm.
Cardiac contusion
Left ventricular hypertrophy
Idioventricular rhythm including paced rhythm
** Brugada syndrome is a genetic disease that is characterised by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death.

64. ST Segment depression
ST SEGMENT DEPRESSION CAN RESULT FROM MULTIPLE PATHOLOGIES, INCLUDING:
Myocardial ischemia
Reciprocal ST segment depression. If one lead shows ST segment elevation then usually the lead 'on the other side' shows ST segment depression. (This is usually seen in ischemia as well.
Left ventricular hypertophy with "strain" or depolarization abnormality
Digoxin effect
Low potassium / low magnesium
Heart rate-induced changes (post tachycardia)
During acute neurologic events.

65. ST Segment depression Morphology of ST Depression
ST depression can be either upsloping, downsloping, or horizontal.
Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia
Upsloping ST depression in the precordial leads is highly specific for occlusion of the LAD.
Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction.
Posterior MI manifests as horizontal ST depression in V1-3 and is associated with upright T waves and tall R waves.

66. T-Wave Inversion
negative (or inverted) T wave> 0.5 mm negative T wave in leads I, II, V3, V4, V5 or V6
Possible causes of T wave changes:
Ischemia and myocardial infarction
Pericarditis
Myocarditis
Cardiac contusion
Acute neurologic events, such as a subarachnoid bleed.
Mitral valve prolapse
Digoxin effect
Right and left ventricular hypertrophy with strain

67. T-Waves
Two characteristics should be always noted with regard to the T wave: inversion and peaked appearance .
Inversion: May represent old infarction or resolving ischemia
Peaked: Electrical instability (i.e. electrolyte imbalance hyperkalemia)

68. Anatomy correlation
EKG leads generally correlate to different anatomical portions of the
Myocardium and the blood vessels that perfuse that region.

69. J point elevation
The J point is where the QRS complex ends and the ST segment begins. J point elevation is a common and usually benign finding on EKG in younger patients.
Early repolarization is a common finding in young, healthy individuals. It appears as mild ST segment elevation that can be diffuse, however is more prominent in the precordial leads. Early repolarization changes are simply “J point” elevation.

70. Pathologic Q Waves
Pathologic Q waves occur when the electrical signal passes through stunned or scarred heart muscle; as such, they are usually markers of previous myocardial infarctions, with subsequent fibrosis.
A pathologic Q wave is defined as having a deflection amplitude of 25% or more of the subsequent R wave, or being > 0.04 s (40 ms) in width and > 2 mm in amplitude. However, diagnosis requires the presence of this pattern in more than one corresponding lead.
Myocardial infarctions with pathological Q waves are referred to as ST elevation MIs.[5]

71. FOLLOW THE STEPS 6. Waveform Morphology Rate Peaked/biphasic P waves
QRS changes
BBB/conduction delay
Low or High Voltage
Pacer
T-waves Inversions
7. ST Segment
Elevation
Depression
8. Q-Waves
Rate
Regularity
Intervals
Rhythm
Axis
Normal
RAD
LAD
No Man’s Land

72. CASE 1 Rate: PR: QRS: Axis: Rhythm: Morphology: ST/T: Q-Waves:
47 year old male presents with chest pain, dyspnea and diaphoresis. Sudden onset.
No prior medical history. No medications. No cardiac risk factors.
HR R – 30 B/P 210/110 Pulse ox 84%
CASE 1
Rate: PR: QRS: Axis:
Rhythm: Morphology:
ST/T: Q-Waves:

73. Rate: 142 PR: 0.12 QRS: 0.06 Axis: LAD
47 year old male presents with chest pain, dyspnea and diaphoresis. Sudden onset.
No prior medical history. No medications. No cardiac risk factors.
HR R – 30 B/P 210/110 Pulse ox 84%
Rate: 142 PR: 0.12 QRS: Axis: LAD
Rhythm: sinus tach Morphology: Peaked P waves/notched
ST/T: T-wave inversion III and T-wave inversion v1-3 Q-Waves: none
This ECG is classic for PE: 1) sinus tach Hypoxia 2) right ventricular conduction delay (R' in V1) 3) T-wave inversions in BOTH precordial leads and in lead III.  4) S1Q3T3 (a tiny R-wave in III is equivalent to a Q-wave). 

74. CASE 2 Rate: PR: QRS: Axis: Rhythm: Morphology: ST/T: Q-Waves:
64 year old male. PMH: HTN DM Lipids PSH 2 ppd x 20 yrs No cardiac hx
Sudden onset dyspnea, diaphoresis, weakness approx 1 hour ago.
Rate: PR: QRS: Axis:
Rhythm: Morphology:
ST/T: Q-Waves:

75. CASE 2 Rate: 100 PR:0.16 QRS: 0.06 Axis: normal to LAD
Rhythm: Sinus tach Morphology: T wave inversion diffuse
ST/T: ST elevation II, III, AVF. ST Depression AVL. V2-5 Q-Waves: II, III, AVF
Dx: acute inferior/lateral wall MI

76. CASE 3 Rate: PR: QRS: Axis: Rhythm: Morphology: ST/T: Q-Waves:
45 Year old male presents for preoperative clearance for hip surgery.
PMH: HTN, Dyslipidemia, Tobacco. Remote cocaine use.
PFH: adopted. PSH: None Works as a truck driver.
HR – 72 B/P 124/78 R-19 BMI -35
Rate: PR: QRS: Axis:
Rhythm: Morphology:
ST/T: Q-Waves:

77. CASE 3 Rate: 98 PR:0.12 QRS: 0.06 Axis: normal
45 Year old male presents for preoperative clearance for hip surgery.
PMH: HTN, Dyslipidemia, Tobacco. Remote cocaine use.
PFH: adopted. PSH: None Works as a truck driver.
HR – 72 B/P 124/78 R-19 BMI -35
CASE 3
Rate: 98 PR:0.12 QRS: Axis: normal
Rhythm: Sinus Morphology: T-wave inversion I, aVL
ST/T: ST elevation III, AVF, V2
Q-Waves: III, V2-V6
Dx: Anterior wall MI (Possible acute), lateral wall (old?)

78. CASE 4 Rate: PR: QRS: Axis: Rhythm: Morphology: Q-Waves: Dx:
HR: 74 Resp: 24 B/P 190/108 Pulse Ox 91%
61 year old female new to practice. Presents for first exam. Denies any medical history but has not seen MD in a decade.
PMH: None PSH: None Meds: None PFH: Colon Ca, stroke, MI
CASE 4
Rate: PR: QRS: Axis:
Rhythm: Morphology:
Q-Waves:
Dx:

79. CASE 4 Rate: 104 PR: 0.10 QRS: 0.06 Axis: normal
HR: 74 Resp: 24 B/P 190/108 Pulse Ox 91%
61 year old female new to practice. Presents for first exam. Denies any medical history but has not seen MD in a decade.
PMH: None PSH: None Meds: None PFH: Colon Ca, stroke, MI
CASE 4
Rate: PR: 0.10 QRS: Axis: normal
Rhythm: Sinus Tach Morphology: Tall QRS anterior leads, Peaked T waves ant. T-wave inversion III, Short PR and peaked P
Q-Waves: None
Dx: Left ventricular hypertrophy with p pulmonale

80. CASE 5 Rate: 104 PR: QRS: Axis: Rhythm: Morphology Short Q-Waves: Dx:
68 year old male, presents with dyspnea for 1 day. Had Substernal chest pain aaprox 8 hours ago.
PMH: HTN Lipids DM PSH 60 pk yr Meds: Atenolol, silfenadil, lipitor, metformin
138/72 HR 58 R-22 Pulse Ox 94%
CASE 5
Rate: PR: QRS: Axis:
Rhythm: Morphology
Short
Q-Waves:
Dx:

81. CASE 6 Rate: 104 PR: QRS: Axis: Rhythm: Morphology Short Q-Waves: Dx:
94 yr old female local ALF, found unresponsive.
No medical history available, patient unresponsive
B/P 84/56 R-28 HR 75 Pulse ox 93%
Rate: PR: QRS: Axis:
Rhythm: Morphology
Short
Q-Waves:
Dx:

82. CASE 7 Rate: 104 PR: QRS: Axis: Rhythm: Morphology Short Q-Waves: Dx:
48 year old male presents for employment physical
PMH: None PSH: None Meds: None
Tobacco: None Recreational drug use : None
Rate: PR: QRS: Axis:
Rhythm: Morphology
Short
Q-Waves:
Dx:

83. CASE 8 Rate: 104 PR: QRS: Axis: Rhythm: Morphology Short Q-Waves: Dx:
64 year old male presents to office because “Doesn’t feel good”
PMH: Htn PSH: None Meds: lisinopril, silfenadil
BP 178/102 HR 54 R-20 Pulse Ox 99%
Rate: PR: QRS: Axis:
Rhythm: Morphology
Short
Q-Waves:
Dx:

84. CASE 9 Rate: 104 PR: QRS: Axis: Rhythm: Morphology Short Q-Waves: Dx:
64 yr old male presents for DMV clearance. Denies any complaints
PMH: None PSH: None Meds: None
Tobacco: remote history Drugs: none
156/95 HR 98 Resp: 24
CASE 9
Rate: PR: QRS: Axis:
Rhythm: Morphology
Short
Q-Waves:
Dx:

85. CASE 10 Rate: 104 PR: QRS: Axis: Rhythm: Morphology Short Q-Waves: Dx:
92 yr old female from nursing home, “confused”
PMH: HTN, CHF, Lipids, DM PSH: CABG
Meds: Metoprolol, lasix, lisinopril, spironolactone
96/48 HR: 60 Resp: 16 Pulse Ox 98%
CASE 10
Rate: PR: QRS: Axis:
Rhythm: Morphology
Short
Q-Waves:
Dx:

86. CASE 10 Rate: PR: QRS: Axis: Rhythm: Morphology Short Q-Waves: Dx:
74 year old male presents for routine follow up/physical exam
PMH: CAD/MI, CABG, HTN, obesity, DM
Meds: glipizide, metformin, lisinopril/hctz
BP 126/80 HR 100 R 24 Pulse ox: 100%
Rate: PR: QRS: Axis:
Rhythm: Morphology
Short
Q-Waves:
Dx: