Download Cardiology / 12 Lead EKG 2016 Advanced EMS Refresher NRP, CCP

Cardiology / 12 Lead EKG
2016 Advanced EMS Refresher
James A Temple BA,
NRP, CCP
Expected Outcomes
• Review basic 12 Lead EKG interpretation
• Using the basic understanding of 12 Lead
EKG, dig a little deeper to pick up and predict
cardiac events and prepare for them.
• Review cases using some of the new
concepts learned.
• WHY?
Is This Stuff Easy?
• Dr Paul Hinchey (Austin-Travis County)
• 12 Lead Over-read?
–
–
–
–
90 total STEMI alerts
87% appropriate to at least 1 cardiologist
43% unanimous “true” stemi
18% unanimous “False” positive STEMI alert
EMS Expectations (Realistic)
• How much training have you had?
• How often do we read 12 Leads?
• What are you really looking for?
Sound like anything else
EMS is dealing with
currently?
Why Do You Have to Be Good at This?
• Decrease time to intervention
– More lives saved
• Why would we let EMS be the weak link in
the chain?
• We CAN make the difference here!
– Pattern recognition
– Predicting events
– Preventing events
12 Lead Review
•
•
•
•
•
•
•
•
•
ST depression
ST elevation
Q Waves
Axis
Reciprocal changes
T-Wave inversion / morphology
R wave progression
BBB
Hemi-blocks
Ischemia
Injury
Infarct
??????
??????
Waveform Components:
Q Wave
First negative deflection
before R wave; Q wave
includes the negative
downstroke & return to
baseline
Waveform Components:
R Wave
First positive deflection; R
wave includes the
downstroke returning to the
baseline
Waveform Components:
S Wave
Negative deflection
following the R wave; S
wave includes
departure from & return
to baseline
Waveform Components:
QRS
• Q waves
– Can occur normally in several
leads
• Normal Q waves called
physiologic
– Physiologic Q waves
• < .04 sec (40ms)
– Pathologic Q
• >.04 sec (40 ms)
See any Q’s?
QTc
A dialysis patient presented with dyspnea and a heart rate of
33. His medications included amlodipine and carvedilol. He
has a history of hypertension and DM. His BP was 150/45
(bradycardia leads to long run-off time after each systolic
beat, leading to low diastolic pressure). He appeared
comfortable, in no distress.
K = 7.5!
Take Homes:
1. Bradycardia should always prompt
consideration of hyperkalemia
2. Bradycardia may be the only ECG
sign of hyperkalemia
Waveform Components:
QRS
• Q wave
– Measure width
– Pathologic if greater than or equal to
0.04 seconds (1 small box)
Q-waves in acute MI:
• 1) QR-waves are common early in anterior MI.
• 2) QS-waves are uncommon early in anterior MI;
they are common in late presentation.
• 3) Q-waves are independently associated with
worse outcomes (78% relative increase in 90-day
mortality in Armstrong et al.)
• 4) Q-waves alone do not necessarily imply
irreversibly infarcted myocardium; they should not
dissuade from reperfusion therapy.
Waveform Components:
QS Complex
Entire complex is
negatively
deflected; No R
wave present
Waveform Components:
J-Point
Junction between end of QRS
and beginning of ST segment;
Where QRS stops & makes a
sudden sharp change of
direction
Waveform Components:
ST Segment
Segment between Jpoint and beginning of
T wave
Waveform Components:
ST Segment
• Need reference point
– Compare to TP segment
– DO NOT use PR segment as reference!
ST
TP
T Wave
• Should measure 5 mm in limb leads
• Should measure 10mm in chest leads
• Concordance
• Should NOT be taller than “R”!!
Hyperacute T-waves are a sign of a large
amount of myocardium at risk and that it is
still viable
Coronary Arteries
• Branch off of the
aorta, just above the
leaflets of the aortic
valve
• Three major arteries
• Each supplies a
specific area
Right Coronary Artery
•
•
•
•
Inferior wall of LV
Right ventricle
Posterior LV
Posterior fascicle of
LBB
• SA and AV node
Left Anterior Descending
•
•
•
•
•
Anterior wall of LV
Septum
Bundle Branches
Hemifascicles
Major pumping mass
of LV
Left Circumflex Artery
• Upper lateral wall of
LV (Leads I and
aVL)
• SA node in 45%
• AV node in 10%
• Posterior wall of LBB
• Posterior
hemifascicle
Lead Groups
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Limb Leads
Chest Leads
Inferior Wall
• II, III, aVF
– View from Left Leg 
– inferior wall of left ventricle
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Inferior Wall
• Posterior View
– portion resting on
diaphragm
– ST elevation  suspect
inferior injury
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Inferior Wall
Lateral Wall
• I and aVL
– View from Left Arm 
– lateral wall of left
ventricle
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Lateral Wall
• V5 and V6
– Left lateral chest
– lateral wall of left ventricle
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Lateral Wall
• I, aVL, V5, V6
– ST elevation 
suspect lateral wall
injury
Lateral Wall
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Anterior Wall
• V3, V4
– Left anterior chest
–  electrode on anterior
chest
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Anterior Wall
• V3, V4
– ST segment
elevation  suspect
anterior wall injury
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Septal Wall
• V1, V2
– Along sternal borders
– Look through right ventricle &
see septal wall
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Septal
• V1, V2
– septum is left
ventricular tissue
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Evolution of AMI
• Hyperacute
– Early change suggestive
of AMI
– Tall & Peaked
– May precede clinical
symptoms
– Only seen in leads
looking at infarcting area
– Not used as a diagnostic
finding
Evolution of AMI
• Acute
– ST segment elevation
– Implies myocardial injury
occurring
– Elevated ST segment
presumed acute rather
than old
Evolution of AMI
• Acute
– ST segment Elevated
– Q wave at least 40 ms
wide = pathologic
– Q wave associated with
some cellular necrosis
Evolution of AMI
• Age Undetermined
– Wide (pathologic) Q
wave
– No ST segment elevation
– Old or “age
undetermined” MI
STE…?
What about the Big Fatties?
A normal 12-lead ECG
DOES NOT mean the
patient is not having
acute ischemia, injury
or infarction!!!
12 Lead Concepts
Lead Groups
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Limb Leads
Chest Leads
Location?
???
???
???
Axis Determination & Deviation
• What is Axis?
– “the general (mean vector) direction of
electrical impulses as they travel through the
heart”
– “the sum total of all electrical currents
generated by the ventricular myocardium
during depolarization”
– normally from upper right to lower left
Axis Determination & Deviation
• What do you need to determine the axis
of an ECG?
– The 12 Lead ECG
– Leads CORRECTLY placed on the patient
•
•
•
•
RA on the right arm
LA on the left arm
LL on the left leg
Not on the chest or abdomen
– Knowledge of axis deviation
What Is Axis?
• Overall direction of
travel of electrical
impulses as they
move through the
heart
• Normal axis is
downward and
toward the left
22
Normal Axis
• Upright complexes in
Leads I, II, III
• Forces going toward
all three leads
• Impulses going
toward a positive,
make a positive
deflection
Physiological Left Axis
• Normal variant in
adults
• Common in obesity
and athletes
• Lead II can show
upward or halfway
deflection
• Lead III is down
Pathological Left Axis
• Disease process
• Suggests anterior
hemiblock
• Patients are 4 times
more likely to arrest
with a hemiblock and
“chest pain”
Right Axis Deviation
• Rare occurrence in
adults
• Almost always
pathological
• Associated with
posterior hemiblock
• Lead I down and
Lead III up
Extreme Right Axis Deviation
• Indeterminate axis
• Usually ventricular in
origin
• Down in all three
leads, I, II, III
To Determine Axis
• Run Leads I, II, and III
• Leads must be on the limbs!
• Look at the net QRS deflection in each
lead (does it go up or down, or halfway)
• Compare to the rapid axis and hemiblock
chart
Calculated Axis Angle
• Machine calculates
this for you
• Use it with your chart
• Look at the “QRS
axis” or the “R axis”
on some units
• Follow the chart
Rapid Axis and Hemiblock Chart
Axis Quadrants
Quadrants
• Left axis
-30 to -90 °
• Normal axis
-30 to 90°
• Right axis
90 to 180°
• Extreme Right
axis or “No
Man’s Land
-90 to 180°
+120°
aVR
-150°
No
Man’s
Land
-90°
-60°
aVL
-30°
LAD
+180°
0° I
Normal
RAD
+30°
+150°
+120°
III
+90°
aVF
+60°
II
Axis Determination
• Quick Axis Determination
– Determine the net QRS deflection in Leads I and aVF
(positive or negative)
Normal
axis
LAD
RAD
ERAD
Lead I
aVF
Axis Practice
ERAD
-90 - 180
RAD
+90 - 180
I
II
III
Axis
HB?
up
up
up
norm
up
up
down
PhysL
up
down
down
Path L
Ant
LAD
-30 - -90
Normal
-30 - +90
down
up
down
Right
Post
down
down
down
ERAD
Vent
Axis Practice
ERAD
-90 - 180
RAD
+90 - 180
I
II
III
Axis
HB?
up
up
up
norm
up
up
down
PhysL
up
down
down
Path L
Ant
LAD
-30 - -90
Normal
-30 - +90
down
up
down
Right
Post
down
down
down
ERAD
Vent
Axis Practice
ERAD
-90 - 180
RAD
+90 - 180
I
II
III
Axis
HB?
up
up
up
norm
up
up
down
PhysL
up
down
down
Path L
Ant
LAD
-30 - -90
Normal
-30 - +90
down
up
down
Right
Post
down
down
down
ERAD
Vent
Axis Practice
ERAD
-90 - 180
RAD
+90 - 180
I
II
III
Axis
HB?
up
up
up
norm
up
up
down
PhysL
up
down
down
Path L
Ant
LAD
-30 - -90
Normal
-30 - +90
down
up
down
Right
Post
down
down
down
ERAD
Vent
Axis Practice
ERAD
-90 - 180
RAD
+90 - 180
I
II
III
Axis
HB?
up
up
up
norm
up
up
down
PhysL
up
down
down
Path L
Ant
LAD
-30 - -90
Normal
-30 - +90
down
up
down
Right
Post
down
down
down
ERAD
Vent
Imposters Checklist
•
•
•
•
•
LVH?
BBB?
Pericarditis?
Early Repolarization?
Paced Rhythms?
Bundle Branch Blocks (BBB)
• So What?
• 25% greater mortality with BBB
• When your QRS measures > 170 ms, your
ejection fraction is below 50%!
• Predictor of those at risk for developing a
CHB.
• New RBBB and STEMI = increased mortality
• V1 and V2 – septal wall (BBB location) –
makes sense anatomically
CONTEXT
• 2-4 % of patients with new LBBB have MI!
• LVH can certainly lead to LBBB!
• Makes it tough, not impossible, to detect MI
with LBBB.
Bundle Branch Block
• Can be pre-existing
condition
• Can be caused by ACS
• If AMI caused
– 60-70% associated with
pump failure
– 40-60% mortality w/o
reperfusion
Bundle Branch Block
Can Mimic or Hide Evidence Needed to
Identify AMI
• May Produce
–
–
–
–
–
ST elevation
ST depression
Tall T waves
Inverted T waves
Wide Q waves
• May Hide
–
–
–
–
–
ST elevation
ST depression
Tall T waves
Inverted T waves
Wide Q waves
Normal Ventricular Conduction
• Normal Conduction
– fibers of LBB begin conduction
– impulse travels across
interventricular septum from left to
right
• towards + electrode creates small r
wave
– travels across ventricles causing
depolarization of both
simultaneously
• LV contributes most to complex
– impulse travels away from +
electrode creates primarily
negative complex
RBBB
• RBBB in V1
– no change in initial
impulse travel
• small r wave
– impulse depolarizes LV
by itself since RBBB
– RV depolarized by
impulse thru muscle
• it now contributes to
complex
– travels toward +
electrode creating
positive deflection
R-S-R´
LBBB
• LBBB in V1
– initial deflection altered
since travels right to left
now
• Q wave or small q wave
– RV depolarizes
unopposed
• may produce small r
wave
– travels across septum to
depolarize LV
• deep S wave
LBBB
• 5-13% of LBBB patients have MI
• LBBB and tachycardia:
– If tachycardia is present with LBBB, it is usually
rate-dependent and resolves once rate is
controlled.
• Underlying rhythm must be
supraventricluar!
Turn signal Theory of BBB
Example: LBBB
Example: RBBB
BBB?
BBB?
BBB?
BBB?
WTH?
• What the heck is a fascicle?
• LBB has 2 (ant / post)
• RBB has one
Hemiblocks
• Posterior fascicle
– Much more difficult to have block  greater
disease
– Less common but more concerning
– Supplies majority of inferior wall of LV
– If blocked, results in right axis deviation
Hemiblocks
• Anterior fascicle
– Easier to have block; More common
– Supplies superior wall of LV
– If blocked, results in pathologic left axis deviation
Hemiblock Identification
• Left Anterior
Hemiblock
– Pathologic Left
Axis Deviation
• small q wave in lead I
• small r wave in lead
III
– Normal QRS or
RBBB
• Left Posterior
Hemiblock
– Right Axis
Deviation
• small r wave in lead I
• small q wave in lead
III
– Normal QRS or
RBBB
• usually does have
RBBB
– “absence of right
ventricular
hypertrophy”
Precursors to Complete Heart Block
•
•
•
•
Any Type II AV Block
Anyone with disease of both bundles
Anyone with two or more of any blocks
Examples:
–
–
–
–
Prolonged P-R & anterior hemiblock
RBBB & anterior hemiblock
RBBB & posterior hemiblock
Prolonged P-R with anterior hemiblock & RBBB
Precursors to Complete Heart Block
• If recognize precursors to CHB, then:
–
–
–
–
Have high index of suspicion for CHB
Have TCP ready (standby mode)
Patient may need a pacemaker
Administration of Lidocaine and other
ventricular antidysrhythmics may result in
CHB
• Lidocaine contraindicated in patients with
precursors to CHB unless TCP in place and ready
Bifascicular Block
• Anterior HB and RBBB
Bifascicular Block
• LBBB
Bifascicular Block
T Wave Morphology with BBB
• Usual QRT waves, in the normal ECG, are
positive in leads I, II and V3 through V6.
– Concordance
• In a LBBB, however, this isn’t true. Because
of the changes in the vector or repolarization,
T waves in a BBB should move in the
opposite direction of the last deflection of the
QRS. This is called “discordance.” To put this
simply, if your QRS leaves you with a
mountain, the T wave should be a valley, and
vice versa.
LVH and T wave deflection
• Concordant positive T waves after a
positive QRS are indicative of ischemia,
and along with ST elevation is one highly
specific sign of AMI in the presence of
LBBB.
• Depression in reciprocal leads would prove
even more definitive. This is important
because LBBB places patients at extremely
high risk for cardiovascular complication.
LVH
• Step 1
– Look in V1 and V2
– Pick the deepest negative deflection (S wave)
– Count small boxes of negative deflection in that lead
– Remember that number
• Step 2
– Look in V5 and V6
– Pick the tallest positive deflection (R wave)
– Count small boxes of positive deflection
– Remember that number
• Step 3
– Add the two numbers together
– Suspect LVH if the sum is > 35 (> 35 mm)
LVH?
Vs. MI?
Benign Early Repolarization (BER)
• Widespread ST elevation
• NO PR segment depression
• Tall, symmetrical and concordant T waves in
the precordial leads. These findings are
classic indicators of BER.
BER
Pericarditis
PR Segment
Depression
Diffuse ST Elevation
(Concave)
Pt history and Exam
Imposter Checklist
• QRS <120 ms?
– Not BBB, not VBR (Paced)
• LVH criteria?
• Early Repol?
– Any reciprocal changes nix BER!
• Pericarditis
– Any reciprocal changes nix Pericarditis!
Concordance
• All V-leads up or
down
• All up: suggestive of
VT but R/O WPW
• All down: suggestive
of VT, R/O LBBB
Assembly
Pifalls in WCT
•
•
•
•
•
Reliance on Lead II
Reliance on the machine
Vital signs/patient presentation
Atrial fibrillation
SVT is more common?
Machine Logic
Clinical Logic/Primary Survey
•
•
•
•
•
•
Is the QRS >120 ms?
Look at axis criteria (can be helpful)
Look at the morphology in Leads V1 and V6
Look for concordance (all up or all down)
Is AV dissociation present?
Patient history/meds
Clinical Logic/Primary Survey
•
•
•
•
•
•
Is the QRS >120 ms?
Look at axis criteria (can be helpful)
Look at the morphology in Leads V1 and V6
Look for concordance (all up or all down)
Is AV dissociation present?
Patient history/meds
First Criteria for VT
• Extreme right axis
• Upright complex in V1 (MCL-1)
• 99% diagnostic for VT
Example of VT
Another Axis Criteria
• Right axis deviation
• Negative V1 (MCL-1)
• 90% specific for VT
Morphology Clues to VT
• Lead V6 (MCL-6)
• Predominately negative deflection in V6
indicates VT
Example: RAD + Negative V1
Patient History
• Two questions:
– Have you had a heart
attack before?
– Did you have fast
heart rates after your
MI?
• If yes to both, odds
of VT are 86% with a
wide complex
tachycardia
Lead V6 Criteria
Capture or Fusion Beats
• Arrow on the 6th complex indicates an escape
beat or fusion beat
• If seen it is diagnostic of VT (AV dissociation)
Example
• 23 y/o male presents with syncope.
• Difficulty finding a baseline EKG…REALLY?
Winter’s T Waves
LAD Occlusion
SWEET
• A 32 yo type I diabetic woman presented with
chest pain, nausea, vomiting and diffuse
abdominal pain. She was in DKA with a
glucose of 1128, and a K of 5.5.
pH = 7.17, pCO2 = 24, HCO3 = 8.
Sweet
Sweet
Sweet Resolution
• 95% LAD occlusion
Doc in the Box
Doc-in-the-Box
• 41 y/o male walked in to clinic for CP
• Evaluated, sent home.
T/P Considerations
Size matters…
• When T towers over R – BEWARE!
• Hyperacute T waves
Importance of Context
CASE
• A male in his 60's with med h/o only
significant for HTN and hyperlipidemia
presented for CP and SOB. On the day prior,
he became very SOB and felt like he was
going to pass out when he tried to stand up
from bed. This was accompanied by chest
heaviness and followed by left chest pain and
a stiff sensation in his neck. The pain
progressed but he went to bed but awoke in
the AM with a heavy and "throbbing" chest.
VS were: 122/92, pulse 82, RR 18, O2sat
(room air) = 95% Here is his initial ED ECG:
There are both precordial T-wave inversions AND Twave inversion in lead III. this is highly suggestive of
pulmonary embolism.
The better we are with 12 Lead EKG, the
more positive impact we will have on the
ultimate goal:
Patient Survival
Atypical
• 41 y/o male
• 3 days of chest discomfort, worsens with
activity.
• CP also associated with Dyspnea
• Wife “requested” him to visit ED
• EKG….
C/C: Dyspnea with assoc CP
Case
• 27 y/o male called 911 for palpitations and
dyspnea.
• No previous hx of cardiac issues.
• Actions:
• What won’t you do?
60 y/o 4 days of CP – some dyspnea
CONTEXT is IMPORTANT
• 40 y/o male with severe asthma attack
• Narrowly avoided intubation
• Routine EKG…
Whadda ya think? AMS, Kussmauling,
hyperglycemic…
• The ECG is diagnostic of hyperkalemia, with
QRS of 180 ms. The QRS improved
immediately after giving 2 doses of Calcium
gluconate. K returned at 7.3, with a pH of
6.91, HCO3 of less than 3. After a total of 5
doses of Ca gluconate, 6 doses of bicarb, 4
liters of fluid, and insulin, this patient with
extremely severe diabetic ketoacidosis
stabilized.
You Make the Call…
• A middle aged man was heard to be falling in
his apartment. He was found very agitated,
intermittently screaming (and on presentation
was intermittently roaring like a lion). There
was no apparent etiology. He required 10 mg
of droperidol for sedation. He underwent an
ECG as a routine part of the evaluation of
possible ingestion:
• Reference value: 440 ms
• 593 ms is dangerously long and may result in torsade
de pointes (polymorphic VT), and could be a result of
the droperidol, or of metabolic and electrolyte
abnormalities, or to many drugs or even be familial.
• In any case, it is unsafe to leave it like this, so we
gave 2 grams of Magnesium. A blood gas revealed
a pH of 7.75 (entirely a respiratory alkalosis, drawn
before intubation and due to his agitation and
hyperventilation), which will also cause long QT and
torsade. K was 3.2, which will also contribute.
• By this time, we had him on the ventilator and so we
intentionally slowed his ventilations to lower the
pH.
Hypokalemia – induced CA!
Hypokalemia EKG’s
• Promotes Torsades!
• Makes sense that Mag Sulfate is indicated!
• Hypocalcemia may also present with
prolonged QT.
Hmmmm…
• 65 yo woman called 911 for pain in her upper
back (between the shoulder blades) and in
the left shoulder and left biceps, and some
"mild chest pressure" elicited by the medics.
Exam was normal. All but the back pain
resolved with nitroglycerine
1730 hrs
• ST depression in aVL is earliest indication of
IWMI!
• V2 ST depression here also suggests
Posterior wall involvement!
1745 hrs
16 y/o female syncope while playing BBall
• A female in her 60s presented with 3 days of
nausea, vomiting, and diarrhea, and not
feeling well. She complained of jaw pain and
shortness of breath. There was a 30 second
episode of syncope, and another one the
previous evening, without any tonic clonic
movements, tongue-biting, or incontinence.
She was ill appearing. She had a remote
history of lung cancer many years ago,
cured. She had no other medical history.
Whadda ya think?
You Can Do This!
• Hypotension
• Shoulder pain
• 3 days of symptoms
• Inferior MI with RV involvement!
Thank You!
[email protected]
1820 hrs
1900 hrs
100% RCA Occlusion
EKG post cath lab
Poor Packer Fan…
Missing anything?
90 minutes later…
Are you sure?
• There is 2-2.5 mm of ST elevation in inferior
leads.
• There is reciprocal ST depression in I and
aVL, with T-wave inversion in aVL.
• There is relative ST depression in V2
• There is ST depression from V3-V6.
• There is a negative T-wave in V3, and
biphasic T-waves in V4-V6.
INFERIOR MI??
OOPS…
• A 23 year old presented with pleuritic left
chest pain radiating to the left arm. He had a
recent sore throat.
REALLY??
• This male in his 40's had been having
intermittent chest pain for one week. He
awoke from sleep with crushing central chest
pain and called ems.
• EMS recorded a 12-lead, then gave 2
sublingual nitros with complete relief of pain.
He arrived in the ED and had this ECG
recorded:
• Active symptoms / pain
Wellens Syndrome
Chicken or the Egg? Pitfalls…
EMS EKG before NTG