1. 12-Lead EKG
MEPN Level IV

2. EISLO’s
Discuss the changes in T wave and ST segment morphology with an MI
List the criteria for identification of right or left bundle branch blocks.
List the anatomically congruent leads associated with an inferior, lateral and anterior wall MI
Describe morphology of Q wave presence

3. Myocardial A&P

4. Heart wall - Three layers
Epicardium (outer)
visceral layer of pericardium
thin, transparent
smooth, slippery
Myocardium (middle)
mass of cardiac muscle
Endocardium (inner)
endothelium over thin connective tissue
smooth lining for the chambers and valves
continuous with blood vessel endothelium

6. Cardiac Enzymes Myoglobin CK Troponin Released by all striated muscle
Rises fast (2 hours) after myocardial infarction
Peaks at hours
Returns to normal in hours CK
Released by all muscles in the body
Rises in 4-6 hours after injury
Peaks in 24 hours
Returns to normal in 3-4 days
CK-MB is myocardial “specific”
Peaks in 3-4 hours
Returns to normal in 2 days
Troponin
More specific for myocardial injury
Rises 2-6 hours after injury
Peaks in 12 hours
Remains elevated for 5-14 days

7. Coronary Blood Flow Arteries first branches off the aorta
blood moves more easily into the myocardium when it is relaxed between beats  during diastole
blood enters coronary capillary beds

8. Collateral Circulation

10. Coronary Circulation

11. Coronary Circulation Pathologies
Compromised coronary circulation due to:
emboli: blood clots, air, amniotic fluid, tumor fragments
fatty atherosclerotic plaques
smooth muscle spasms in coronary arteries
Problems
ischemia (low supply of nutrients)
hypoxia (low supply of O2)
infarct (cell death)

12. Internodal tracts Bundle of His Right Bundle Branch
Cell specialization – pacemaker cells, transmission cells
Sino-Atrial (SA) Node: natural cardiac pacemaker. The heartbeat starts here and spreads throughout the network of conduction fibers in the two atria causing them to contract.
Normally, the heartbeat can only reach the ventricles (the two lower chambers), after it has passed through the atrioventricular (AV) node.
Atrioventricular (AV) Node: slows down the electrical signal so that the atrial contractions can finish filling the ventricles completely. The AV node also prevents the lower chambers from beating too fast if the atria develops a fast rhythm (tachyarrhythmia).
Function
Impulse creation
Impulse transmission
Organized and coordinated
Characteristics
Interwoven throughout myocardium
Innervation by direct cell to cell contact
Right Bundle
Branch

13. SA Node Cardiac muscle cells are involuntary, striated, branched
Each fiber is connected to the others by intercalated discs

14. Intranodal Pathways
Anterior, middle and posterior pathways. Bachman’s bundle in the right transmits through the inter-atrial septal region

15. AV Node Conduction Normal conduction pathway from atria to ventricles
Limits number of atrial impulses sent to the ventricles
In the Wall of the right atrium next to the opening of the coronary sinus and the septal leaflet of the tricuspid valve

16. Bundle Branches HIS bundle – only route
LAF – anterior and superior aspects; single strand
LPF – fan-like, posterior and inferior aspects; more difficult to block
His Bundle, bundle branches, and the Purkinje system : The electrical signal finally passes to the ventricles causing the ventricles to contract

17. Action Potential Phase 0 Phase 2 Phase 3 Phase 1 Phase 4 Plateau phase
Begins at -70 mV with a slow influx of sodium ions; gradually raising the potential toward threshold
When threshold is reached fast sodium channels open; causing the cell to fire
Phase 1
Rapid sodium pumps are slowed by influx of potassium
Phase 2
Plateau phase
Sodium influx slows; calcium begins to enter the cell
Calcium stimulates cellular contraction by stimulating the myocyte
Phase 3
Reverse pumps open; rapid repolarization
Phase 4
Back to the -70 mV resting potential
Ion movement affects what happens electrically in the heart
Medications are given to effect ion movement
Lidocaine – Na+
Calcium channel blockers K+

18. Myocardial Action Potential
Depolarization
Phase 1 of the action potential
Stimulation of the cardiac cell by the pacemaker cell causing an influx of Na and Ca, outflow of K.
Repolarization
Phase 2 of the action potential
No impulse entering the cells can cause it to depolarize
Relative refractory period
Phase 3 of the action potential
Impulses entering the cardiac cell now can cause serious, uncontrolled reactions.
Absolute refractory period
Phase 4 of the action potential
The return of the cardiac cells to resting state.
One cardiac contraction, A single ventricular contraction

19. EKG Basics 25 mm per sec Each small box - horizontally = 0.4 sec
Each small box - vertically = 1 mm
Horizontal marks time
Vertical marks amplitude

20. EKG Review - Analysis Rhythm Rate P waves P-R Interval QRS complex
Regular or irregular
Rate
Too fast, too slow, just right
P waves
Upright, inverted, not there, not related
P-R Interval
; >0.20; <0.12
QRS complex
<0.12
QT Interval
P Wave
P wave should be upright in Leads I and II as well as V3-V6
P wave always inverted in aVR
P wave usually upright in aVF and V3 but occasionally biphasic or flat
P wave is variable in leads III,  aVL, V1 and V2 (upright, inverted, biphasic)
Most people say that your best view of the P wave is in Lead II – others say V1. The truth is that every patient is different, find the best one on your patients EKG and study that one well.

21. Normal .04 to .12 seconds in width
P wave: Represents positive and negative deflections of atrial contraction and relaxation
PR Interval: Distance between the P wave and the Q/R wave
QRS Complex: represents ventricular depolarization
Q wave: First negative deflection
R Wave: First positive deflection
S Wave: second negative deflection
ST Segment: Essentially isoelectric, slopes gently upward
Normal > .08 sec
J point: the point where the S wave meets the isoelectric line
T Wave: Ventricular repolarization
always upright in leads I, II, V2-V6
aVR is always negative.
Leads III, aVL, aVF, and V1 can be positive or negative
U Wave: unclear etiology, commonly seen in V2-V3 due to proximity to ventricular mass; common in bradycardia, hypokalemia, digitalis
PR interval <.12 is indicative of preexcitement – re-entry problem or atrial dysfunction
Normal .04 to .12 seconds in width
Factors altering Amplitude
Men have larger amplitudes than women
Young people have higher amplitude than elderly
Precordial amplitudes are higher than limb leads
Causes of QRS widening
Ventricular Rhythms
BBB

22. QT interval QTc QT corrected for heart rate QT / R-R = QTc
beginning of the QRS complex to the end of the T wave represents ventricular depolarization and repolarization ---- Changes with heart rate
QTc
QT corrected for heart rate QT / R-R = QTc
Evaluates the recovery of the ventricle
Manual verification should be used when computer generation is long
Range is
Normal: 0.39 men; 0.41 women
Age and gender dependent, 10 articles will you give you 10 different normal ranges
Can be affected by:
Drugs
Cardiomyopathy
Hypothermia
Congenital QT lengthening is not well defined but is thought to be the cause of sudden death in young adults (athletes) as the HR increases the next R can land on the T
Prolonged QTc associated with Torsades
Bazettes formula used to calculate QTc, four formulas that can be used

23. ECG Leads 6 limb leads (frontal plane) 3 bipolar leads
3 unipolar leads
6 precordial leads (horizontal plane)
V1 – V6

24. Einthoven’s Triangle Limb Leads BIPOLAR Lead I RA (-) to LA (+)
Lead II
RA (-) to LL (+)
Lead III
LA (-) to LL (+)

25. AUGMENTED (UNIPOLAR) LEADS
Augmented leads combine 2 leads together (the null point) from the center point of the triangle with one positive pole.
aVR (Augmented Voltage Right Arm positive) is a combination of bipolar Leads I and II
aVL (Augmented Voltage Left Arm Positive) is a combination of I and III
aVF (Augmented Voltage Left Foot positive) is a combination of Bipolar Leads II and III

26. II, III & AVF
WHAT ARE THE LEADS
LOOKING AT?
I & AVL
LIMB and AUGMENTED
LEADS

27. Precordial Lead Placement
V1 – 4th intercostal space right of sternum
V2 - 4th intercostal space left of sternum
V4 – 5th intercostal space midclavicular line
V3 – midway between V2 and V4
V6 – 5th intercostal space midaxillary line
V5 – same level as V4 at anterior axillary line between V4 and V6

28. Same lead position as left side –
RIGHT SIDED EKG
Same lead position as left side –
looks directly at the
Right ventricle

29. Posterior View Posterior leads:
V7 – lateral to V6 at posterior axillary line
V8 – level of V7 at the mid-scapular line
V9 – level of V8 at the paravertebral line
(left posterior thorax midway from spine to V8)
Posterior View

31. PRECORDIAL LEADS
V1 & V2
V3 & V4
V5 & V6

32. Bottom line is continuous strip
calibration marker
LIMB LEADS
AUGUMENTED
LEADS
PRECORDIAL LEADS
Bottom line is continuous strip

33. R – Wave Progression

34. R – Wave Progression

35. Myocardial infarction
Myocardial ischemia
Various definitions are used. The term commonly refers to diffuse ST segment depression, usually with associated T wave inversion
Myocardial injury
Injury always points outward from the surface that is injured with ST segment elevation
Myocardial infarction
death of heart muscle

36. Ischemia, Injury, Infarction Waveforms

37. ST segment should be electrically neutral

38. Visual aid in determining:
Ischemia or injury to myocardium
Normal should be at baseline
Depressed ST segment - >2 mm below baseline

40. EKG 1

41. ST Segment Elevation
ST segment elevation is attributed to impending infarction
but can also be due to pericarditis or vasospastic (variant) angina.
The height of the ST segment is measured at a point 2 boxes after the end of the QRS complex
significant if it exceeds 1 mm in a limb lead or 2 mm in a precordial lead.

42. EKG 2

43. T Waves T waves are normally positive in leads with a positive QRS
T waves are normally asymmetrical
T waves are normally not more than 5 mm high in limb leads or 10 mm high in precordial leads or 2/3 the height of the R wave

44. T wave
Ischemia
Hyperkalemia
Ischemia
Ischemia

45. Hyperkalemia
EKG 3

46. ST-T Wave Combination of infarction and often hyperkalemia
Called Tombstone ‘T’ because of the shape.
Usually a sign of impending cardiac death.

47. Inferior-Anterior-Lateral
EKG 4

48. Pathology of an MI

49. Localization of ECG Pathology
Inferior: Abnormalities that appear in leads II, III, and aVF (called the inferior leads) indicate pathology on the inferior or diaphragmatic surface of the heart.
Lateral: Leads I, aVF, and V5-V6 are called lateral leads. Abnormality in these leads indicates pathology on the lateral, upper surface of the heart.
Anterior: Anterior pathology is seen in leads V1-V4, and often in lead I.

50. Possible loss of R wave in
Overview of Infarcts
Location of Infarct
Arterial Supply
Indicative Changes
Reciprocal Changes
Anterior
LAD
V1-V4
II, III, aVF
Inferior
RCA
I, aVL
Lateral
Circumflex
V5, V6 V1
Posterior
Posterior Descending (RCA)
V7, V8, V9 - elevation
V1, V2 -ischemia
Septal
Septal Perforating (LAD)
Posterior Descending (RCA
Possible loss of R wave in
V1, V2, V3
None

51. T Wave Elevation T
ST Segment Elevation ST ST Q T
Pathological
Q Wave Q Q T
T Wave Inversion

52. EKG Changes from Infarction
First Detectable Change in EKG
Tall T-waves
increase in height
more symmetric
may occur in the first few minutes
Hyper-acute Phase

53. Acute Phase ST Segment Elevation Primary indication of injury
Occurs in first hour to hours
ST Segment Elevation in Leads
1mm or greater in limb leads
2 mm or greater in chest leads
Hallmark indication of AMI

55. CASE STUDY – EVOLUTION of MI

65. View of Inferior Heart Wall
Leads II, III, aVF
Looks at inferior heart wall

66. Inferior
EKG 5

67. Inferior
EKG 6

68. *Sometimes referred to as High Lateral or High Apical view*
View of Lateral Heart Wall
Leads I and aVL
Looks at lateral heart wall
Looks from the left arm toward heart
*Sometimes referred to as High Lateral or High Apical view*

69. View of Lateral Heart Wall
Leads V5 & V6
Looks at lateral heart wall
Looks from the left lateral chest toward heart
*Sometimes referred to as Low Lateral or Low Apical view*

70. View of Entire Lateral Heart Wall
Leads I, aVL, V5, V6
- Looks at the lateral wall of the heart from two different perspectives
Lateral Wall

71. Lateral
EKG 7

72. Lateral
EKG 8

73. View of Anterior Heart Wall
Leads V3, V4
Looks at anterior heart wall
Looks from the left anterior chest

74. Anterior
EKG 9

75. EKG 10

76. View of Septal Heart Wall
Leads V1, V2
Looks at septal heart wall
Looks along sternal borders

77. Putting it ALL together
ANTERIOR
LATERAL S E P T A L
LATERAL
LATERAL
INFERIOR

78. Q Waves Definition Septal depolarization
Normally present in I, aVL, V6

79. Two types of Q waves Non-pathologic Pathologic Narrow, shallow Q waves
Not visible in all leads
Pathologic
> 0.04 in duration; at least 1/4 to 1/3 height of R wave
Represent an infarcted area of myocardium

80. PATHOLOGICAL Q WAVES

81. Bundle Branch Blocks
If the QRS duration is > .12
there is usually an abnormality of conduction of the ventricular impulse

82. RBB Block
Most common ventricular conduction defect
Can be acute or chronic
Acute RBBB is associated with an acute anterior MI

83. EKG 11
RBBB

84. LBB Block
Always indicates a diseased heart
More common in older adults

85. EKG 12
LBBB