April 2007 CE Cardiology and 12-Lead EKG`s
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Transcript April 2007 CE Cardiology and 12-Lead EKG`s
Cardiovascular
Emergencies and
12 Lead EKG’s
Condell Medical Center
EMS System
April 2007
Site Code #10-7200E-1207
Prepared by:
Sharon Hopkins, RN, BSN, EMT-P
Objectives
Upon successful completion of this
program, the EMS provider should be
able to:
–understand the normal anatomy &
physiology of the cardiovascular
system
–describe anatomical changes to the
heart during ischemic episodes
–differentiate presentations of patients
with cardiorespiratory complaints
–describe lead placement for
obtaining a 12 lead EKG
–recognize ST elevation on
the 12 lead EKG
–identify and appropriately state
interventions for a variety of
dysrhythmias
–actively participate in discussion of
case presentations
–successfully complete the quiz with
a score of 80% or better
Cardiovascular System
This
system is composed of the heart
and blood vessels
Delivers oxygenated blood to all cells
Transports hormones throughout the
body
Transports waste products for waste
disposal
The heart is a pump
–right pump is under low pressure
–left pump is under high pressure
Components of Circulatory
System
Functioning heart
Sufficient blood volume
Intact blood vessels
If any one of the above 3 are not
working properly, the patient may be
symptomatic and could be in need of
intervention
Blood Flow Through The Body
Systemic
circulation
Left ventricle
Aorta
arteries
arterioles
capillaries
venules
veins
Right atrium
Superior
vena cava
Right
atrium
Right
ventricle
Aorta
Left
atrium
Left
ventricle
Myocardial Blood Flow
The
heart is a muscle (myocardium)
3 layers
epicardium - smooth outer surface
myocardium - thick middle layer,
responsible for cardiac contraction activity
endocardium - innermost layer of thin
connective tissue
Myocardial
blood flow
– via coronary arteries immediately off aorta
– heart is the 1st structure to receive
oxygenated blood - it’s that important!
Coronary Arteries
Left
main coronary artery
–left anterior descending coronary
artery (LAD)
supplies left ventricle, septum
–circumflex coronary artery
supplies left atrium, left
ventricle, septum, part of right
ventricle
Right coronary artery (RCA)
supplies right atrium & ventricle
Coronary Blood Flow
Influences of Heart Function
Preload
– pressure under which a ventricle fills; volume
of blood returning to fill the heart
Afterload
– the resistance the ventricle has to pump
against to eject blood out of the heart
– the higher the afterload the harder the
ventricle has to work
Ejection
fraction (EF)
– percentage of blood pumped by the ventricle
with each contraction (healthy >55%)
– damage to heart muscle decreases EF
Problems That Affect
& Afterload
Preload
Preload
Afterload
increased oxygen
arteriosclerosis
demand increases
induced high B/P
volume of blood
can cause left
returning to heart
ventricle to
become exhausted
temporarily not a
& stop working
problem
efficiently
heart enlarges when
preload remains
increased (FrankStarling law)
Problems That Decrease
Ejection Fraction (EF)
Myocardial
infarction (MI)
Congestive heart failure (CHF)
Coronary artery disease (CAD)
Atrial fibrillation
Cardiomyopathy
Anemia
Excess body weight
Poorly controlled blood pressure
CO = SV x HR
CO
- cardiac output
– amount of blood pumped by the heart in
one minute (normal 5-6 L/min)
SV
- stroke volume
– amount of blood pumped out by either
ventricle in a single contraction (normal
60-100 ml)
HR
- heart rate
– number of cardiac contractions per
minute (normal pulse rate 60-100/min)
CO = SV x HR
A change in stroke volume or heart rate
will affect cardiac output
SV and HR = CO
– ie: compensatory mechanism
SV and steady HR = CO
– ie: preload = afterload (ie: shock in
patient taking beta blockers)
SV and HR = CO
– ie: patient with symptomatic tachycardia
steady
SV and HR = CO
– ie: patient with symptomatic bradycardia
Coronary Artery Disease (CAD)
Leading
cause of death in USA
– Narrowing or blockage in coronary artery
decreasing blood flow
– Atherosclerosis - thickening & hardening of
the arteries due to fatty deposits in vessels
– Plaque deposits build up in arteries
arteries narrow
arteries become blocked
blood clots form
Overtime,
CAD can contribute to heart
failure & dysrhythmias
Collateral Circulation
Development
of new blood vessels to
reroute blood flow around blockage
in a coronary artery
New arteries may not be able to
supply enough oxygenated blood to
heart muscle in time of increased
demand
Ischemia occurs when blood supply
to the heart is inadequate to meet
the demands
Coronary Artery Disease (CAD)
Plaque in a coronary artery breaks apart
causing blood clot to form and blocks artery
Defining
Acute Coronary Syndrome
Types
of CAD related to sudden rupture
of plaque inside a coronary artery
unstable angina
non-ST segment elevation MI
(NSTEMI)
ST segment elevation MI (STEMI)
Length of time blood flow blocked and
amount of damage determines type of
acute coronary syndrome
Symptoms of Cardiovascular
Problems
Breathing
problems
– Shortness of breath (SOB)
– Paroxysmal nocturnal dyspnea (PND)
suddenly
awakens with
shortness of breath
–Orthopnea
dyspnea when lying down
–Breath sounds
are clear or not clear?
Peripheral
edema
–excess fluid found in tissues of the
most dependent part of the body
presacral
area in bedridden person
feet and ankles in someone up and about
Syncope
–fainting when cardiac output falls
–fainting while lying down is considered
cardiac in nature until proven otherwise
Palpitations
–sensation of fast or irregular heartbeat
Pain
Initial Impression
Not
necessarily important to know
exactly what to “name” the patient’s
problem (diagnosis)
Important to identify signs and
symptoms that need to be treated
Important to recognize the possible
medical condition the signs and
symptoms may be representing
Important to determine the right
treatment approach
Patient Assessment:
OPQRST of Pain Symptoms
Onset
– Sudden or gradual?
– Anything like this before?
Provocation
or palliation
– What makes it better/worse?
– What was the patient doing at the time?
Quality
– What does it feel like (in patient’s own
words)?
Radiation
– From where to where?
Severity
– How bad is it on a scale of 0-10?
Timing
– When did it start
– How long did it last?
– Continuous or intermittent?
Vital Signs: Tools for Pt Assessment
Heart
rate
–too fast
ventricle
does not stay open long
enough to adequately fill
–too slow
rate
too slow to pump often enough to
maintain an adequate volume output
Blood
pressure
–could be elevated in anxiety and pain
–low in shock
–serial readings (trending) tell much
Respirations
– Abnormally fast, slow, labored, noisy?
Clear - hear breath sounds enter & exit
Crackles - pop, snap, click, crackle
fluid in lower airways
Rhonchi - rattling sounds; resembles
snoring
mucus in the airways
Wheezes - whistling sound; initially
heard on exhalation
narrowing airways (ie: asthma)
Absence of sound - not good!!!
Pulse
oximetry (SaO2)
–Measures percent of saturated
hemoglobin in arterial blood
–<95% indicates respiratory
compromise
–<90% indicates dire problem
–Need to evaluate reading with
patient’s clinical presentation do they match?
Inaccurate SaO2 Readings
Hypotensive or cold patient (falsely
low)
Carbon monoxide poisoning (falsely
high)
Abnormal hemoglobin (sickle-cell
disease) (falsely low)
Incorrect probe placement (falsely low)
Dark nail polish (falsely low)
Anemia (falsely high - whatever
hemoglobin patient has is saturated)
EKG
monitoring
– Indicates electrical activity of the heart
– Evaluate mechanical activity by measuring
pulse, heart rate and blood pressure
– Can indicate myocardial insult and location
ischemia - initial insult; ST depression
injury - prolonged myocardial hypoxia or
ischemia; ST elevation
infarction - tissue death
–dead tissue no longer contracts
–amount of dead tissue directly relates
to degree of muscle impairment
–may show Q waves
ST depression
ST elevation
Q wave
Acute Coronary Syndrome
Variety of events that represent acute
myocardial ischemic pain (plaque rupture)
Unstable angina
Intermediate severity of disease between
stable angina and acute MI; tissue ischemia
Non-Q wave infarct (NSTEMI)
No ST elevation but MI is present with
tissue necrosis (death)
Q wave infarct (STEMI)
ST elevation MI with tissue necrosis (death)
Usually a large/significant infarct
Initial Treatment
Acute Coronary Syndrome
Regardless
of the end diagnosis, all
patients treated initially the same
– IV-O2-monitor-vital signs-history
– aspirin
– nitroglycerin
– morphine if necessary
– 12 lead EKG obtained & transmitted
Treatment
fine-tuned as more
diagnostic information is obtained
Acute Myocardial Infarction
Coronary
blood flow deprived so that
portion of muscle dies
– occlusion by a thrombus (blood clot
superimposed on ruptured plaque)
– spasm of coronary artery
– reduction in blood flow (shock,
arrhythmias, pulmonary embolism)
Location
and size of infarct depends on
which coronary artery is blocked &
where
– left ventricle most common
AMI Signs & Symptoms
Chest
pain - most common especially
in men
– lasts >15 minutes
– does not go away with rest
– typically felt beneath sternum
– typically described as heavy, squeezing,
crushing, tight
– can radiate down the arm (usually left),
fingers, jaw,upper back, epigastrium
Pain
not influenced by coughing,
deep breathing, movement
Atypical AMI Signs & Symptoms
Persons with diabetes, elderly, women,
and heart transplant patients
Atypical presentation - from drop in
cardiac output (CO)
– sudden dyspnea
– sudden lose of consciousness (syncope)
or near-syncope
– unexplained drop in blood pressure
– apparent stroke
– confusion
– generalized weakness
Atypical AMI Signs & Symptoms
Women
– nausea
– lightheadedness
– epigastric burning
– sudden onset weakness
– unexplained tiredness/weakness
Women
at greater risk
– symptoms ignored (by patient & MD)
– under-recognized
– under-treated
Congestive Heart Failure
Heart
unable to pump efficiently
Blood backs up into systemic system,
pulmonary system or both
– Right heart failure
most often occurs due to left heart failure
can occur from pulmonary embolism
can occur from long-standing COPD (esp
chronic bronchitis)
– Left heart failure
most commonly from acute MI
also occurs due to chronic hypertension
Right Heart Failure
Blood
backs up into systemic circulation
– gradual onset over days to weeks
– jugular vein distension (JVD)
– edema (most visible in dependent parts of
the body) from fluids pushed out of veins
– engorged, swollen liver due to edema
– right sided failure alone seldom a life
threatening situation
Field treatment most often symptomatic
More aggressive treatment needed when
accompanied with left heart failure
Left Sided Heart Failure
Heart
unable to effectively pump
blood from pulmonary veins
Blood backs up behind left ventricle
Pulmonary veins engorged with blood
Serum forced out of pulmonary
capillaries and into alveoli (air sacs)
Serum mixes with air to produce
foam (pulmonary edema)
Progression Left Heart Failure
Think
“left - lungs”
Impaired oxygenation
– compensates by respiratory rate
Fluid
leaks into interstitial spaces
– auscultate crackles
interstitial pressure narrows bronchioles
– auscultate wheezing
Dyspnea
& hypoxemiapanicrelease of
adrenalineincreased work load on heart
Left Heart Failure
Sympathetic
nervous system response
– Peripheral vasoconstriction
peripheral resistance (afterload) increases
weakened heart has to pump harder to
eject blood out through narrowed vessels
blood pressure initially elevated to keep up
with the demands and to pump harder
against increased vessel resistance
diaphoretic, pale, cold skin
Asthma or Heart Failure?
Asthma
Left heart failure
younger patient
older patient
hx of asthma
poss hx heart problems
unproductive cough orthopnea
meds for asthma
recent rapid weight gain
wheezing
cough with watery or
foamy fluid
accessory muscles
being used
meds for heart problems
wheezing
JVD
Pedal or sacral edema
Which Came First - CHF or AMI?
Often
hard to determine which came first
and triggered the development of the
other problem
Heart failurepoor perfusion &
hypoxemiamyocardium suffers from
inadequate blood & oxygen supplyacute
myocardial ischemiaacute coronary
syndrome
AMIpoor pumping performance of
heartacute failure of left heart pumpleft
heart failure
Not
unusual to see the AMI patient in
pulmonary edema - watch for it!
Cardiogenic Shock
Heart
extensively damaged; it can no
longer function as a pump
25% of heart damage causes left
heart failure
>40% of the left ventricle is
infarcted, cardiogenic shock occurs
High mortality rate
Signs & Symptoms
Cardiogenic Shock
Altered
level of consciousness
– confusion to unconsciousness
Restless,
anxious
Massive peripheral vasoconstriction
– pale, cold skin, poor renal perfusion
Pulse
rapid and thready
Respirations rapid and shallow
Falling blood pressure
Treatment Goals
Acute Coronary Syndrome
Goals
– early recognition of a possible cardiac
problem
– minimize size of infarction
– reduce myocardial oxygen demand
– decrease patient’s fear & pain
(minimizes sympathetic discharge)
– salvage ischemic myocardium
– prevent development of dysrhythmias
– improve chances of survival
Acute Coronary Syndrome
Oxygen
– may limit ischemic injury
Aspirin
- 324 mg chewed
– blocks platelet aggregation (clumping)
to keep clot from getting bigger
– chewing breaks medication down faster
& allows for quicker absorption
– hold if patient allergic or for a reliable
patient that states they have taken
aspirin within last 24 hours
Nitroglycerin
0.4 mg sl every 5 minutes
– dilates coronary vessels to relieve vasospams
– increases collateral blood flow
– dilates veins to reduce preload to reduce
workload of heart
– if pain persists after 2 doses, move to
Morphine
Morphine
- 2 mg slow IVP
– decreases pain & apprehension
– mild venodilator & arterial dilator
reduces preload and afterload
–2mg slow IVP repeated every 2 minutes
as needed, max total dose 10 mg
Treatment Goals
Congestive Heart Failure
Goals
– improve oxygenation
– decrease workload of the heart
(ie: preload & afterload)
Treatment Stable Acute
Pulmonary Edema (B/P>100)
Nitroglycerin
- 0.4 mg sl
– Vasodilator to create venous pooling
– Reduces preload & afterload
– Maximum 3 doses (repeated every 5
minutes)
Consider
CPAP - use if indicated
Lasix - 40 mg IVP
– Diuretic - excess fluid excreted via kidneys
– Venodilating effect to pool venous blood
– Dose to 80 mg IVP if patient on Lasix
Morphine
- 2 mg slow IVP
– Venodilator to increase pooling of blood
– Anxiolytic to calm anxious patient
– May repeat 2mg dose every 2 minutes
– Maximum total dose 10 mg
Albuterol
- 2.5 mg/3ml nebulizer
– Wheezing may indicate
bronchoconstriction from excessive fluid
– Bronchodilator could be helpful
Hypotensive
side effects
– Treatment used (NTG, Lasix, Morphine,
CPAP) can all cause venodilation B/P
Treatment Unstable Acute
Pulmonary Edema (B/P<100)
Contact
Medical Control
CPAP on orders of Medical Control
Consider Cardiogenic Shock Protocol
If wheezing (indicating
bronchoconstriction), contact Medical
Control for Albuterol order
– if patient needs to be intubated, Albuterol to
be delivered via in-line
Treatment Goals
Cardiogenic Shock
Goals
– Improve oxygenation
– Improve peripheral perfusion
– Avoid adding any workload to the heart
Treatment Cardiogenic Shock
Oxygen
via nonrebreather mask
– BVM if respirations ineffective
– Intubation may become necessary
Positioning
– Supine if lungs are clear
– Head somewhat elevated if pulmonary
edema is present (semi-fowler’s)
IV/IO
fluid challenge in 200ml
increments if lung sounds are clear
– The shock may include a hypovolemic
component
Treatment Cardiogenic Shock
Cardiac
monitor
– Arrhythmias are likely
May cause hypotension decreasing cardiac
output
Dopamine
Infusion - maintain B/P >100
– Effects dose related & dependent on clinical
condition of patient
–5 - 20 g/kg/min has beta influence on
the heart
Increases
contractility strength of heart
To a lesser degree increases heart rate
Dopamine
cont’d
– Doses >20g/kg/min
Alpha stimulation predominate &
vasoconstriction my negatively affect
circulation
Extravasation
- leaking out of vessels
– Can cause tissue necrosis
– Report IV infiltration to ED staff & document
Dosing
- start at 5 g/kg/min
– Refer to table in SOP page 13 OR
– Take patient’s weight in pounds, take 1st 2
numbers, & subtract 2 (ie: 185 pounds:
18 - 2 = 16 gtts/min to start drip)
EKG Monitoring & 12 Lead EKG’s
Goal
EKG monitoring
– Identify a disturbance in the normal cardiac
rhythm
– Arrhythmias caused by
Ischemia
Electrolyte imbalances
Disturbances or damage in electrical
conduction system
Goal
of obtaining 12 lead EKG
– Early recognition Acute Coronary Syndrome
Treat
clinical condition, not the monitor!
12 Lead EKG’s
Obtain
and transmit to Medical
control when you are following the
Acute Coronary Syndrome SOP
Many patients can be monitored by a
Lead II but not all patients need a 12
lead.
Some patients experiencing angina
or an acute MI will not yet have any
EKG changes indicated on the 12
lead.
A normal EKG DOES
NOT necessarily
mean there is
nothing acute going
on!
Cardiac Conduction System
SA
node - dominant pacemaker
– upper right atrium
– blood supply from RCA
Internodal
pathways
– to spread electrical impulse thru-out atria
AV
node in region of AV junction
– in 85-90% of people, blood supplied by
RCA to AV node
– in 10-15% of people, blood supplied by
left circumflex
Conduction System cont’d
bundle
of His
Right and left bundle branches
Purkinje fibers - through ventricular
muscle
Changes in electrolyte concentrations
influence depolarization and
repolarization
sodium (Na+), potassium (K+),
calcium (Ca++), Magnesium (Mg++)
Conduction System
L
l Left bundle
branches
EKG Wave Forms
P
wave
– depolarization of atria
PR
interval
– depolarization of atria & delay at AV
junction
– normal PR interval 0.12 - 0.20 seconds
QRS
complex
– depolarization of ventricles
– normal QRS complex <0.12 seconds
T
waves
– repolarization of ventricles (and atria)
EKG Wave Forms
The J Point
J point - end of QRS complex & beginning
of ST segment
ST segment elevation - evaluated 0.04
seconds after J point
Acute Myocardial Infarction
Acute myocardial infarction (AMI) is part of a
spectrum of disease known as acute coronary
syndrome (ACS)
ACS
– Larger term to cover a group of clinical
syndromes compatible with acute myocardial
ischemia
– Chest pain is due to insufficient blood supply
to the heart muscle that results from
coronary artery disease (CAD)
– Clinical conditions include unstable angina to
non-Q wave MI and Q wave MI
Preparation for 12 Lead EKG
Patient
preparation
– Relatively hairless surface
clip hair if necessary so electrodes adhere
– Clean and dry skin surface
gently rub skin area with gauze pad
need to remove skin oils & dead skin
if diaphoretic patient wipe with
towel/gauze or use antiperspirant
deodorant spray
Patient
positioning
– Preferably flat; if elevated note on EKG
12-Lead Placement
Utilizes
10 electrodes
attached in specific
locations
4 standard limb leads
RA (right arm)
LA (left arm)
LL (left leg)
RL (right leg)
Limb
leads should be
placed on limbs
Precordial Chest Leads
For every person, each precordial lead
placed in the same relative position
V1 - 4th intercostal space, R of sternum
V2 - 4th intercostal space, L of sternum
V4 - 5th intercostal space, midclavicular
V3 - between V2 and V4, on 5th rib or in
5th intercostal space
V5 - 5th intercostal space, anterior
axillary line
V6 - 5th intercostal space, mid-axillary
Precordial
Leads
Lead Placement
The
more accurate the lead
placement, the more accurate the
12-lead interpretation
12-leads are often evaluated on a
sequential basis, each interpretation
considering the previous one
V4-6 should be in a straight line
12 Lead Printout
Standard
format 81/2 x 11 paper
12 lead views printed on top half
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
Additional single view of rhythm strips
usually printed on bottom half
Machines can analyze data obtained
but humans must interpret data
Limb Leads (Bipolar)
Lead I - views the
left (lateral) side of
heart
Lead II - views the
bottom (inferior)
side of heart
Lead III - another
inferior view of the
heart
Limb Leads
(Unipolar)
aVR
- view from
right arm
aVL - lateral view
from left arm
aVF - inferior
view from left leg
Precordial (Chest) Leads
Views the
septal,
anterior,
& lateral
portions
of the
heart
Heart in the Thoracic Cavity
Myocardial Insult
Ischemia
– lack of oxygenation
– ST depression or T wave inversion
– permanent damage avoidable
Injury
– prolonged ischemia
– ST elevation
– permanent damage avoidable
Infarct
– death of myocardial tissue
– may have Q wave
Evolution of AMI
A - pre-infarct
B - Tall T wave
C - Tall T wave & ST
elevation
D - Elevated ST,
inverted T wave,
Q wave
E - Inverted T wave,
Q wave
F - Q wave
ST Depression
Can
indicate
ischemia
electrolyte abnormality
rapid heart rate
digitalis influence
reciprocal changes to ST elevation
ST
depression measurement
– 1 mm (1 small box) below baseline
measured 2 mm (2 small boxes) after
end of QRS
ST elevation
is more
significant so
should be
looked for in
opposite
leads when
depression
noted
T Wave Inversion
T wave represents ventricular repolarization
– Normally upright in all leads except V1 and aVR
Inverted T waves tend to represent
ischemia
Note
T wave
inversion
aVL,
V4 -6
ST Segment Elevation
Finding
indicates injury or damage
Injury probably due to occluded
coronary artery
Muscle can still be salvaged
If corrective intervention not taken in
timely manner, tissue necrosis/death is
likely (infarction)
TIME IS MUSCLE!
Significant ST Elevation
ST
segment elevation measurement
– 0.04 seconds after J point
ST
elevation
– > 1mm (1 small box) in 2 or more
contiguous chest leads (V1-V6)
– >1mm (1 small box) in 2 or more
anatomically contiguous leads
Contiguous
lead
– limb leads that “look” at the same area
of the heart or are numerically
consecutive chest leads
Contiguous Leads
Inferior
wall: II, III, avF
Lateral wall: I, aVL, V5, V6
Septum: V1 and V2
Anterior wall: V3 and V4
Posterior wall: V7-V9
(leads placed on the patient’s back
5th intercostal space creating a 15
lead EKG)
ST Segment Elevation
Coved
shape
usually
indicates
acute
injury
Concave
shape is
usually
benign if
patient is
asymptomatic
Groups of EKG Leads
Inferior
wall - II, III, aVF
Septal wall - V1, V2
Anterior wall - V3, V4
Lateral wall - I, aVL, V5, V6
aVR
is not evaluated in typical groups
Standard lead placement does not look
at posterior wall or right ventricle of
the heart - need special lead placement
for these views
Pathological Q Waves - Infarction
Death
of tissue
Pathological Q wave
–>0.04 seconds wide or
– 1/3 of R wave height
–when seen with ST elevation
indicates ongoing myocardial
infarction
Remember: ST segment probably
single most important element on EKG
when looking for evidence of AMI
Pathological Q Wave
Acute MI Locator Table
Location
Leads
Reciprocal
changes
Inferior
(RCA)
Septal
(LAD)
Anterior
(LAD)
Lateral
(Circumflex)
II, III, aVF
I, aVL
V1, V2
V3, V4
II, III, aVF
V5, V6, I,
aVL
II, III, aVF
Common Complications of AMI
V1-2:
septal wall - infranodal
heartblock, BBB
V3-4: anterior wall - LV dysfunction,
CHF, BBB, 3rd degree HB, PVC’s
I, aVL, V5-6: lateral wall -LV
dysfunction, AV nodal block in some
II, III, aVF: inferior & posterior wall
LV - hypotension, sensitivity to
Nitroglycerin & Morphine
Reciprocal Changes
Changes
seen in the wall of the heart
opposite the location of the infarction
Observe ST segment depression
Usually observed at the onset of
infarction
Usually a short lived change
Lead
Reciprocal changes
II, III, aVF
I, aVL
I, aVL, V5, V6
II, III, aVF
V1-V4
V7-V9
Practice Identifying ST Segment
Elevation
> 1mm (1 small box) in 2 leads from any
group or 2 or more contiguous leads
(>2 mm (2 small boxes) in limb leads
considered alternative elevation by some)
measured 0.04 seconds after J point
Practice Identifying
Leads Showing ST
Elevation
Evaluate the top 3 rows of the
12-lead EKG
Additional rows run rhythm strips
Think Pattern Recognition
Inferior Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Think Pattern Recognition
Lateral Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Think Pattern Recognition
Anterior Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Think Pattern Recognition
Septal Wall MI
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
Test Yourself What pattern would indicate an
anterior/septal wall MI?
I
Lateral
aVR
V1
Septum
V4
Anterior
II
Inferior
aVL
Lateral
V2
Septum
V5
Lateral
III
Inferior
aVF
Inferior
V3
Anterior
V6
Lateral
ST Elevation II, III, aVF
Inferior Wall Involvement
ST Elevation V5, V6, aVL - Lateral
ST Elevation V1-V4 - Ant/Septal
ST Elevation II, III, aVF, V6
Inferior & Lateral Wall
ST Elevation I, aVL, V2-6
ST Elevation II, III, aVF
Case Discussion #1
66
year-old male presents with
“indigestion” for past 2 hours,
frequent belching, nausea, paleness,
diaphoresis, left arm discomfort
Vital signs
– 102/76
What
HR 98
RR 20
SaO2 98%
is your impression and what
initial treatment is indicated?
Case #1
Impression:
possible AMI
SOP: Acute Coronary Syndrome
Treatment:
– IV-O2-monitor-pulse ox
– Vitals stable
– History unremarkable
– Aspirin chewed (any contraindications?)
– Nitroglycerin sl (ask about Viagra use)
– Morphine if pain unrelieved after 2 NTG
– 12 lead to ED for interpretation
Case #1 12-Lead
Case #1
Impression
of 12 lead?
– no ST segment elevation noted
Does
lack of ST segment elevation
change field treatment for this
patient?
– Normal EKG does not preclude that
acute myocardial event is occurring
– Acute Coronary Syndrome SOP to be
followed
Case Discussion #2
77
year-old female with history of
CABG, hypertension, cholesterol, and
long standing diabetes
Presents with vague complaints of not
feeling well, very tired & no energy over
the last day
Meds:
–Aspirin, Isoptin, Toprol,
Hydrochlorothiazide, Lipitor,
Glucophage
Case #2
Vitals:
110/72 HR-72 RR-18 SaO2 97%
Monitor (lead II rhythm strip):
Case #2
What
is your initial impression?
Need to at least consider possible MI
Remember:
–women, elderly, and long standing
diabetics report the most atypical
complaints
Remember:
–a lead II only looks at one view of
the heart
–a normal EKG does not rule out AMI
Case #2
Treatment:
–IV-O2-monitor-vitals
–Aspirin appropriate?
–Nitroglycerin indicated?
–12 lead EKG necessary?
–What about antidysrhythmic for the
PVC’s?
call
Medical Control for guidance
oxygen is often enough to suppress
PVC activity
Case #2
Aspirin
– if patient reliable and took own dose within
last 24 hours, can omit, document why
omitted and when taken
Nitroglycerin
– patient not having chest pain. Defer to
Medical Control for orders
– no contraindications noted (B/P >100; no
viagra type drug used within past 24 hours
- ask, don’t assume!)
12
lead should be obtained on high
index of suspicion
Case #3
81
year-old female complaining of
shortness of breath for past 2 days.
Unable to tolerate lying flat; JVD noted
History of CHF, angina, arthritis, and mild
COPD
Vitals:126/92 HR-170 RR-24 SaO2 97%
Medications: nitroglycerin PRN,
– Lasix 40 mg daily
– Potassium
– Aspirin, one daily
– Proventil inhaler PRN
Case #3 - What is this rhythm?
Rhythm
Case #3
Rapid atrial fibrillation
Initial impression?
Rapid atrial fibrillation
heart rate ineffective pumping
cardiac output
Treatment
initiated
IV-O2-monitor-vitals-history
Goal of therapy - slow down heart rate
Is patient stable or unstable?
– Stable - B/P >100, alert & cooperative
Case #3
ALS
Treatment
– If Diltiazem not available, then what?
Verapamil
– 5 mg IVP slowly over 2 minutes
– If no response after 15 minutes and B/P
remains >100, repeat 5mg slow IVP
Carefully
monitor patient for
development of further deterioration
and increased difficulty breathing
Position of comfort - usually sitting up
Verapamil / Isoptin®
Action
Calcium channel blocker
Slows conduction thru AV node to
control ventricular rate
Relaxes vascular smooth
muscle
Dilates coronary arteries
Verapamil
Indications
Alternative to Diltiazem/cardizem
SVT not responsive to 2 doses of
Adenosine - to terminate rhythm
Stable rapid atrial flutter/fibrillation to control heart rate
Dosing
5 mg IVP slowly over 2 minutes
If no response after 15 minutes and
B/P >100, may repeat Verapamil 5 mg
IVP slowly over 2 minutes
Verapamil
Side Effects
Headache, dizziness
B/P from vasodilation
nausea & vomiting
Contraindications
B/P
Wide complex tachycardias of uncertain
origin
Heart block without implanted pacemaker
WPW, short PR & sick sinus syndromes
Case #4
32
year-old male patient with
complaints of chest tightness, shortness
of breath, and just not feeling well for
past 2 days. Also states sore throat and
ear pain. Very anxious & scared.
No history, no meds
Jogs 2-3 miles 5 times per week
Vitals: 110/70 HR-68 RR-20 SaO2 98%
Lungs clear; skin warm, dry & pink
Case #4
Initial
impression
Cardiac?
Musculoskeletal (what has patient
been doing)?
Viral illness (sore throat & ear pain)?
What treatment would you begin?
Cardiac - can give Aspirin but call
Medical Control for NTG or Morphine
Normal EKG cannot rule out ACS
process
Case #5
68
year-old male called 911 due to
non-radiating chest discomfort (not
relieved with 3 of the patient’s own
nitroglycerin) with some minor
shortness of breath
History:
– stable angina
– GERD
– hypertension (controlled with medications)
– Type II diabetic (recently diagnosed)
Case #5
Allergies
- aspirin
Medications
– nitroglycerin PRN
– isordil
– nexium
– verapamil
– glucophage
Vital
signs
– 136/78 HR-78 RR-18 SaO2 99%
What
is your initial impression & what
treatment is initiated?
Case #5
Initial impression: acute coronary syndrome
IV-O2-monitor-vitals & history
Lead II EKG strip:
You have just hooked the patient for a 12lead EKG and they grabbed their chest and
became unresponsive
Case #5
What
is this rhythm strip?
What
action needs to be taken by EMS?
Case #5
Confirm
no breathing, no pulse
Begin CPR until the defibrillator is ready
and is charged to maximum joules
Clear the patient & deliver 1 shock
Immediately resume CPR for 2 minutes
(5 cycles of 30:2)
Check rhythm, defibrillate
Meds: vasopressor (Epinephrine)
antidysrhythmic (choose 1)
1 shock in between meds & 2 min CPR
VF/Pulseless VT Meds
Epinephrine
1mg every 3-5 minutes
IV/IO for duration of arrest
Antidysrhythmic:
Amiodarone 300 mg IV/IO 1st dose
OR
Lidocaine 1.5 mg/kg IV/IO 1st dose
Repeat dose antidysrhythmic x1 in 5 min:
Amiodarone 150 mg IV/IO
OR
Lidocaine 0.75 mg/kg IV/IO
Antidysrhythmics in VF/VT
Amiodarone
to the vein)
needs to be diluted (irritable
– total of 20 ml syringe (med mixed with
saline)
– rapid push in VF/VT (slow if pt has pulse!)
Lidocaine
-
– if unsuccessful defibrillation
contact Medical Control for 3rd dose order
– if defib successful & bolus given < 10 min,
begin drip 2mg/min (30 mcgtts)
– if defib successful & bolus given >10 min,
give Lido 0.75 mg/kg IV/IO & start drip
Case #5
The patient was defibrillated twice and
received 1 dose of epinephrine
After the 3rd shock, 2 minutes of immediate
CPR resumed
After 2 min of CPR, what is the rhythm?
Case #5
Rhythm:
sinus rhythm
EMS action?
– Determine if there is a pulse (yes!!!)
– Reevaluate airway, breathing, circulation-B/P
– Medications:
because no antidysrhythmic were given,
need to call Medical Control for direction
if Lidocaine, usually 0.75 mg/kg IV/IO
if Amiodarone, 150 mg diluted into 100 ml
bag D5W; run thru mini-drip tubing; run
piggyback at rapid drip over 10 minutes
May not want any antidysrhythmic given
Medication Administration
6
medication rights
right patient
right medication (check 3 times)
right dose
right time
right route
right documentation (time, drug, dose,
route, response)
ETT Route
Endotracheal
tube route is
discouraged, not eliminated.
Absorption found to be unpredictable
ETT route
L - Lidocaine
E- Epinephrine
A- Atropine
N - Narcan
Double
the calculated amount for the
IV/IO route
SOP Test
Will
be given during May, 2007 CE
Similar to November, 2006 SOP
exam
Will test knowledge of entire SOP
Start to review revised SOP’s now
No Jeopardy before the May test
Bibliography
American
Heart Association Guidelines
CPR ECC 2005
Beasley, B., West, M. Understanding 12Lead EKG. Pearson Ed, 2001.
Caroline, Nancy. Emergency Care in The
Streets, Jones & Bartlett, 2008.
Page, B. 12-Lead EKG, Pearson, 2005.
Phalen, T, Aehlert, B. The 12-Lead EKG
in Acute Coronary Syndromes, 2006.
www.clevelandclinic.org
www.nhlbi.nih.gov/health/dci/Diseases