Transcript 12 lead MEPN IV

12-Lead EKG
MEPN Level IV
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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
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Myocardial A&P
http://www.healthline.com/vpvideo/how-the-heart-works
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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
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Cardiac Enzymes
•
Myoglobin
– Released by all
striated muscle
– Rises fast (2 hours)
after myocardial
infarction
– Peaks at 6 - 8 hours
– Returns to normal in
20 - 36 hours
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•
Troponin
–
–
–
–
More specific for
myocardial injury
Rises 2-6 hours after
injury
Peaks in 12 hours
Remains elevated for 5-14
days
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
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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
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Collateral Circulation
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Coronary Circulation
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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)
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Internodal tracts
Bundle
of His
Right
Bundle
Branch
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SA Node
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Intranodal Pathways
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AV Node Conduction
Normal conduction pathway from
atria to ventricles
Limits number of atrial impulses
sent to the ventricles
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Bundle Branches
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Action Potential
Phase 0
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
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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.
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EKG Basics
25 mm per sec
Each small box - horizontally = 0.4 sec
Each small box - vertically = 1 mm
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EKG Review - Analysis
Rhythm
Regular or irregular
Rate
Too fast, too slow, just right
P waves
Upright, inverted, not there, not
related
P-R Interval
0.12-0.20; >0.20; <0.12
QRS complex
<0.12
QT Interval
.34-.44
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P wave: Represents positive and negative deflections of
atrial contraction and relaxation
PR Interval: Distance between the P wave and the Q/R
wave .12 -20
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
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QT interval
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
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ECG Leads
• 6 limb leads (frontal plane)
– 3 bipolar leads
– 3 unipolar leads
• 6 precordial leads (horizontal plane)
– V1 – V6
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Einthoven’s Triangle
Limb Leads
BIPOLAR
Lead I
RA (-) to LA (+)
Lead II
RA (-) to LL (+)
Lead III
LA (-) to LL (+)
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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
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WHAT ARE THE
LEADS
LOOKING AT?
I & AVL
II, III & AVF
LIMB and AUGMENTED
LEADS
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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
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RIGHT SIDED EKG
Same lead position as left side –
looks directly at the
Right ventricle
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Posterior leads:
Posterior View
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)
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PRECORDIAL LEADS
V1 & V2
V3 & V4
V5 & V6
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calibration marker
LIMB LEADS
AUGUMENTED
LEADS
PRECORDIAL LEADS
Bottom line is continuous strip
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R – Wave Progression
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R – Wave Progression
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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
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Ischemia, Injury, Infarction
Waveforms
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ST
Segments
ST segment should be electrically
neutral
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• Visual aid in
determining:
– Ischemia or
injury to
myocardium
– Normal should
be at baseline
– Depressed ST
segment - >2
mm below
baseline
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EKG 1
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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.
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EKG 2
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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
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T wave
Ischemia
Hyperkalemia
Ischemia
Ischemia
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Hyperkalemia
EKG 3
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ST-T Wave
• Combination of infarction and often
hyperkalemia
• Called Tombstone ‘T’ because of
the shape.
• Usually a sign of impending cardiac
death.
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Inferior-Anterior-Lateral
EKG 4
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Pathology of an MI
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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.
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Overview of Infarcts
Location of
Infarct
Arterial
Supply
Indicative
Changes
Reciprocal
Changes
Anterior
LAD
V1-V4
II, III, aVF
Inferior
RCA
II, III, aVF
I, aVL
Lateral
Circumflex
I, aVL
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
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T Wave
Elevation
T
ST
Segment
Elevation
ST
ST
Q
T
Pathological
Q Wave
Q
Q
T
T Wave
Inversion
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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
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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
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CASE STUDY – EVOLUTION of MI
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View of Inferior Heart
Wall
Leads II, III, aVF
- Looks at inferior
heart wall
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Inferior
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EKG 5
Inferior
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EKG 6
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*
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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*
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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
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Lateral
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EKG 7
Lateral
EKG 8
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View of Anterior Heart Wall
• Leads V3, V4
– Looks at anterior
heart wall
– Looks from the left
anterior chest
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Anterior
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EKG 9
7510
EKG
View of Septal Heart Wall
Leads V1, V2
- Looks at septal
heart wall
- Looks along sternal
borders
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Putting it ALL together
ANTERIOR
LATERAL
S
E
P
T
A
L
LATERAL
LATERAL
INFERIOR
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Q Waves
• Definition
– Septal depolarization
– Normally present in I, aVL, V6
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Two types of Q
waves
– Non-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
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PATHOLOGICAL Q WAVES
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Bundle Branch Blocks
If the QRS duration is > .12
there is usually an abnormality of
conduction of the ventricular
impulse
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RBB Block
Most common ventricular
conduction defect
Can be acute or chronic
Acute RBBB is associated
with an acute anterior MI
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EKG 11
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RBBB
LBB Block
Always indicates a
diseased heart
More common in
older adults
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EKG 12
LBBB
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