Transcript 12 Lead-ACS - Fleming College

12 Lead-ACS
Fleming College
Paramedic Program
Focus of ACS
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Common reason for transport
Much can be done during transfer
Reduce risk of morbidity and mortality
The first step = recognizing the ACS
 Signs
and symptoms
 ECG changes
 Biochemical changes
Summary
Strategies for reducing morbidity and
mortality
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Reduce cardiac workload
Improve perfusion to cardiac tissue
Reduce risk of fatal arrhythmias
Reduce extension of clot formation
Reperfuse the ischemic myocardium
Myocardial Infarction
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ASA (2 x 80 mg) P.O.
O2 therapy
IV access
NTG via SL, transdermal, and/or IV
Morphine
Heparin and/or Beta blockers
12 Lead ECG as soon as possible
Pre-hospital Thrombolysis
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Air Ambulance-Ornge
Oshawa Land ALS
Positive empirical trends
Pre-hospital Thrombolysis
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prolonged transport time
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no thrombolysis at the sending facility
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Long delays
Indications - Thrombolysis
 Ischemic
 Less
C.P.
than 12 hours duration
Ischemic Chest Pain?
O - at rest or with exertion
P – better or worse
Q - heaviness, tightening, sharp,
weakness etc
R - neck, jaw and/or left arm
S - varies
T - consistent, does NOT come & go
12 Lead ECG Criteria
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ST segment elevation
New onset Left Bundle Branch Block
with S&S?
Some acute coronary syndromes
(A.C.S.) do not benefit from
thrombolysis
LBBB-FYI ONLY!
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Cannot reliably
diagnose AMI in the
setting of a LBBB
Collaborative data
(history, enzymes
etc.) in the setting
of a new LBBB is an
indication for
thrombolysis
What are the Benefits?
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Varies between subgroups of patients
Time to thrombolysis
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“Infarct to Drug Time”
shorter the better the
outcome
Its all about Timing
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Thrombolytics within one
hour of onset of CP - 50%
reduction in infarct size
Thrombolytics within two
hour of onset of CP - 30%
reduction in infarct size
Thrombolytics within 3-4
hour of onset of CP - 13%
reduction in infarct size
TIME IS MUSCLE - after 6-12 hours less helpful
Examples of Thrombolytics
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Retaplase
Tenectoplase (TNK)
Streptokinase
Tissue plasmingen activator (TPA)
Absolute Contraindications for
Thrombolytics
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Aortic dissection
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Active (significant) bleeding
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Pericarditis
Relative Contraindications
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CPR >10 minutes
Pregnancy
Uncompressible puncture site (from
IV etc)
Age (>75)
Recent surgery or trauma or stroke
(>2 wks)
Current use of warfarin or other
anticoagulant
Aortic Dissection
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How to not get fooled
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CP radiating into back
Tearing vs pressure
Unequal pulses or blood pressures in
limbs
Neurological symptoms
Hypertension ++ (or low if they are
leaking)
CXR
Things to do BEFORE
Thrombolysis
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Venipunctures
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CXR
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Blood analysis
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INR, aPTT, CBC
etc.
Explain
risk/benefits to
patient
Pericarditis
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How not to get fooled?
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Non-specific CP - sometimes severe
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ST segment elevation (ah..ha! But
where?)
Pericarditis
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How to not get fooled
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Atypical ischemic CP
Sitting forward can decrease discomfort
Fever or systemic illness
Younger without cardiac risk factors
ST elevation is diffuse, no anatomical
pattern
Serial ECG’s
Active Bleeding
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Non-compressible site(s)
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most common are GI and GU
More Relative Contraindications
The grey area
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intracranial/intraspinal surgery
intracranial neoplasm, A-V malformation,
aneurysm
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bleeding diathesis
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severe hypertension
What is the Risk?
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Intracranial hemorrhage
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Overall rate - 0.9%
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Varies considerably between patients
What is the Risk?
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Baseline risk w/o RF - 0.75%
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2-3% up to 5% in anterior
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As low as 1% in inferior
What is the Risk?
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Age > 65 add 0.5%
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Add another 0.5%
> 75 y.o.
 >80 y.o.
 >85 y.o.
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What is the Risk?
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SBP > 160 add 0.5%
SBP > 180 add another 0.5%
Weight < 70 kg add 0.5%
Any previous stroke add 2-4%
In the right patient the risk is
significant
All
stroke
risks!!
Other Treatment Options
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ASA
Heparin
Beta Blockers
IIB/IIIA inhibitors
Primary PTCA
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Best option in patients with
increased risk or in patients with
limited benefit
Potential for ambulances close to
these centers (tertiary care centres)
e.g Peterborough, Kingston,
toronto, Ottawa
Percutaneous Transcoronary Angiography
(PTCA)
Success
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Approx. 70% of patients regain
patency of the vessel
Pain relief
Reduction in ST segment deviation
Arrhythmia's
Access
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Specialty procedure
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Rescue angioplasty (fast transfers!!)
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high risk for thrombolytics Rx
thrombolytics failed to correct the problem
Post Thrombolytic Care
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Watch for reperfusion arrhythmias
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Usually benign
Usually transient
Watch for signs of bleeding
Watch for signs of bleeding!
Now to the 12 lead bit….
Introduction to 12 Lead ECG
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Diagnostic 12 lead is performed
to rule in/out various pathologies
Standard limb leads (I,II,III)
Augmented vector leads
(aVL,aVR, aVF)
Precordial or chest leads
The Importance of a 12 lead EKG
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Many calls involve
the CVS
12 lead ECG is a
useful tool in the
cardiac assessment.
What Can be Assessed on the 12 lead
EKG?
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Axis
Bundle branch conduction
Hypertrophy
Fascicular conduction
Ischemia/Injury/Infarction patterns
Pericarditis
Electrolyte disturbances
Drug intoxication
AND MUCH MUCH MORE!!!!!
Required Skills to Interpret the 12 lead
EKG
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Comprehension of electrophysiology
 electrolyte and cellular functions during
normal and abnormal de/repolarization
Advanced knowledge of cardiac
pathophysiology
Recognizing normal versus abnormal
Ability to follow an organized and sequential
approach
LOTS AND LOTS OF PRACTICE!!!!!
Fundamentals of 12 Lead Interpretation
Review
of cardiac
conduction
Refresh the
understanding of the
anatomy and physiology
applicable to EKG
interpretation
Cardiac Conduction
Sinoatrial node
Right atrium
 Near superior
vena cava
 Depolarizing
the atria
through
intranodal
tracts
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Cardiac Conduction
Atrioventricul
ar node
Right atrium
 Near the
septum
 Mediates
conduction
to the
ventricles
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Cardiac Conduction
Bundle of His
Originates in
the AVN
 Left and right
branches
 Spreads action
potential
throughout
ventricles
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12 Lead EKG - Limb Leads
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Lead I
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Lead II
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Right arm to left
arm
Left positive
Right arm to
Left leg
Left leg positive
Lead III
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Left arm to Left
leg
Left leg positive
12 Lead EKG - Limb Leads
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Bipolar leads
form
Einthoven’s
triangle
Reference
points are the
lead origins
This is
important !
12 Lead EKG - Augmented Leads
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Augmented lead
right (aVR)
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Origin point to the
right
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Augmented lead
left (aVL)
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Origin point to the left
Augmented lead
foot (aVF)
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Origin point downward
12 Lead EKG - Augmented Leads
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Unipolar leads form
Goldberger’s triangle
Origin point is the heart
This is an important
reference!
A tip: imagine this
triangle within the
Einthoven’s triangle!
The 6 Limb Leads
I 0°
II +60 °
III +120 °
aVL -30 °
aVR -150 °
aVF +90 °
What Part of the Heart?
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Frontal plane leads look at different
segments of the heart
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Know what area the leads focus on
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Relationship
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Leads II, III and aVF view the
inferior wall
Leads I and aVL view the lateral
wall
Lead aVR is not helpful here
Purpose of the 12 Lead
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Identify ST elevation/depression
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T wave inversion
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Identify VT in wide complex rhythms
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Electrical axis and hypertrophy
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Bundle branch blocks
Indications?
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Ischemic chest pain (unstable angina)
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Chest pain – NYD
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Change in chest pain presentation
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To rule out cardiac involvement
Rule of Thumb
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Perform a 12-lead when considering
differential diagnoses
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It
It
It
It
could
could
could
could
be
be
be
be
angina
an MI
an aneurysm
pericarditis
Don’t do it unless you are prepared (or
someone else is) to act on the result!
Precordial Leads - 12 Lead
Precordial Leads - How are they
placed?
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V1 - 4th intercostal space, R sternal
border
V2 - 4th intercostal space, L sternal
border
V4 - 5th intercostal space,
midclavicular line
V3 - between V2 and V4
V6 - 5th intercostal space, midaxillary
line
V5 – anterior axillary line between V4
and V6
The 6 Chest Leads
12 Lead ECG - LP 12
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Attach limb leads as per
normal
Attach precordial leads
to multi-lead adapter
Attach to patient as per
prior diagram
Press ’12 lead’ button
DON’T TOUCH PATIENT
DURING NEXT 20-30
SECS. ASK PATIENT
NOT TO MOVE
Receive 12 lead from
Printer
12 Lead ECG
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Each of the 12 leads views the left
ventricle from the positive electrode
In the precordial leads, it is
assumed this is in the center of the
heart
Review 12 lead information in Bledsoe
Myocardial Infarction
The BIG ONE!
Lead Perspective
 Lead
I and aVL = lateral wall
 Lead
II, III and aVF = inferior wall
 aVR
is not helpful here
 V1
and V2 = anterior-septal wall
 V3
and V4 = anterior wall
 V5
and V6 = lateral wall
ST Segment Deviation
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ST segment is typically isoelectric
ST segment represents total ventricular
depolarization
ST segment changes are caused by
cellular changes
Causes of ST segment changes
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During ischemia the resting membrane
potential is lowered
 relative ST segment elevation
Asynchronous depolarization of multiple
cardiac cells
 true ST segment elevation
Criteria for Cardiac Injury on the
EKG
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Transmural cardiac injury
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Limb ST segment elevation of 1mm
and extending at least 2mm out from
the J point
Precordial ST segment elevation of
2mm
Other findings may include
 Inverted or flipped T waves
 Pathological Q waves
Phases of an Acute MI
Hyper acute phase
- ST segment elevation begins in the first hours
and
may last 1-6 weeks
Evolved phase
- deep T waves and onset of pathological Q
waves
Resolution phase
- T waves return to normal morphology and
position
Chronic phase
- pathological Q waves
How can we determine the affected
vessels?
The left coronary
artery
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bifurcates into
two primary
branches
circumflex artery
left anterior
descending
Determining the Affected Vessels?
The right coronary
artery
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right atria & ventricle
inferior wall of the
left ventricle
2/3 of the posterior
wall
How can we determine the affected
vessels?
Observe the vessel
mapping!
Knowledge Application!
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Is there any
ST segment
deviation?
What leads
are affected?
What area
do these
leads look
at?
Reciprocal Changes
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ST changes opposite from the
anatomical location of the
injured region
‘mirror-like’ image
ST segment depression is
reciprocal to ST elevation
Investigate further to rule out/in
injury pattern
Practice!
Differential Diagnosis - ST Segment
Elevation
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Acute myocarditis
Hyperkalemia
Hypothermia
Acute cor pulmonale
Cerebrovascular hemorrhage
Cardiac tumor
Even occasionally in healthy
individuals!!!
Ischemia
Electrophysiology - Ischemia
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Cells quickly lose O2 and nutrient
supply
CO2 removal is impeded
Unable to completely repolarize
ECG
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depressed ST segment and/or
inverted T waves
T waves = ventricular repolarization
ST depression of 2mm or greater =
pathology
Other Multi-lead ECG
Configurations
15 lead ECG
and
18 lead ECG
Right Side EKG
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To provide a more specific look at
the right ventricle
Leave V1 in place - this becomes V2R
Leave V2 in place - this becomes V1R
Move V4 to the 5th ICS on the right
midclavicular line = V4R
Move V3 halfway between V2R and V4R =
V3R
Move V5 to the right anterior axillary line
in the 5th ICS = V5R
Move V6 to the right midaxillary line =
V6R
Posterior EKG
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To provide a closer look at the
posterior wall of the heart
Move 3 precordial leads to the same
horizontal plane as
V5 & V6
Be sure to note which leads you have
repositioned
 Position them at the bottom of the left
shoulder blade left of the vertebral
column
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Utility of a 12 Lead ECG
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It is only as good as the
interpretation
Treat the patient first!
Start with the basics - O2, NTG, MS,
IV etc.
Closely monitoring patients with
suspected ACS
Practice Practice
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Google it!
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Buy a book
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Try it on everyone in EMERG with
chest pain!
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