mod_i-12_lead_ekgs.ppt

CMC EMS System
ECRN CE
12 Lead EKG’s
Mod I 2009 CE
Prepared by:
Sharon Hopkins, RN, BSN

Objectives
 Upon successful completion of this module,
the ECRN will be able to accomplish the
following:
 Identify the appropriate components of the
cardiac conduction system with the correct
wave form on a rhythm strip.
 Identify when it is appropriate to obtain an EKG
 Identify the criteria for significant ST elevation.
 Identify EKG leads that view the anterior,
inferior, lateral walls, and septum

Objectives
 Recognize the patterns of an MI after viewing the
components of a 12 lead EKG
 Identify typical and atypical presentations of AMI
 Identify complications associated with an inferior wall MI
 Identify complications associated with an anterior/septal
wall MI
 Identify complications associated with a lateral wall MI
 Identify interventions for complications related to heart
block, pulmonary edema, and cardiogenic shock
 Identify the SOP guidelines for the patient presenting with
acute coronary syndrome as written in the Region X
SOP’s

Objectives
 State dosing and precautions for Aspirin,
Nitroglycerin, and Morphine in the Region X SOP’s.
 Identify ED staff expectations of EMS personnel when
calling the hospital to report a patient with ST
elevation identified on a 12 lead EKG
 Identify EMS expectations when delivering a patient
to a hospital after ST elevation has been identified on
a 12 lead EKG
 Given a picture, correctly trace the order of the
cardiac conduction system.
 Given a picture, correctly identify electrode placement
to obtain a 12 lead EKG.

Why Are We doing Pre-hospital
EKG’s?
 Early recognition and fast, appropriate
treatment can prevent the extension of an
MI
 Early recognition = early intervention
 An important diagnostic tool will also be
the patient’s general appearance

Cardiac Conduction System
 Electrical cells arranged in a systematic
pathway
 Predominant pacemaker starting the
electrical flow comes from the SA node
 Electrical cells are part of the conduction
system
 Muscle cells are the mechanical cells

Cardiac
Conduction
System
Purkinje
fibers
1
2
3
4
5
4

EKG Waveforms
 P wave represents atrial stimulation
 P wave is rounded and upright
 PR interval
 Includes the P wave and the isoelectric PR
segment
 PR interval is the time it takes for an impulse
to travel from the SA node through the
internodal pathways toward the ventricles
 Includes delay time in the AV node
 Normal PR interval is 0.12 – 0.20 seconds

PR
Interval
Normal
0.12 –
0.20
seconds

PR Interval Abnormalities
 PR interval <0.12 seconds
 Impulse did not begin in the normal
pacemaker site of the SA node but
somewhere in the atria
 PR interval >0.20 seconds
 There was a longer than normal delay
transmitting the impulse through the AV node
 A change in the PR interval measurement
generally will not make the patient symptomatic

EKG Wave Forms cont’d
 QRS complex
 Consists of the Q, R, and S waves collectively
 Represents ventricular depolarization or discharge of
electrical energy throughout ventricular muscle
 Larger than the P wave because ventricular
depolarization involves a larger muscle mass than
atrial depolarization
 Palpation of a pulse is generated by ventricular
depolarization (seen as the QRS complex)
 Normal timing usually considered between 0.06
and 0.11 seconds
 Normal is less than 0.12 seconds

QRS Complex Measurement
 From beginning of Q wave – usually fairly
straight forward
 Stop measurement at end of S wave; not
necessarily where QRS intersects baseline
 On S wave, watch for small notch or other
indicator that electrical flow is changing
Not always so easy to determine stop point
 Do not include ST segment or T wave
 Abnormally wide QRS indicates delay in
conduction time through the ventricles

EKG Wave Forms cont’d
 T wave
 Represents ventricular repolarization
 Repolarization is the phase of electrical activity
where electrical charges (influenced primarily
by sodium (Na+) and potassium (K+)) return to
their original state and prepare to respond to
the next electrical charge received
 Atria repolarize during ventricular depolarization
so the small atrial T wave is hidden during the
larger QRS complex

When To Obtain a 12-Lead EKG
 Any patient presenting with signs and/or
symptoms of an acute coronary syndrome
Consider atypical AMI presentations
 Elderly
 Women
 Patient with long standing history of
diabetes
 Any patient presenting with a Second degree
Type II (classical) or 3rd degree heart block
 Consider the origin of heart block from an AMI
until proven otherwise

What Are We Looking For?
 Abnormalities that indicate interruption in the
blood flow to the myocardium
 Plaque formation diminishes blood flow
through the coronary arteries
Patients may be asymptomatic while
damage silently develops
 Plaque rupture begins a cascade of events
that further compromises blood flow through
the injured vessel(s)
 This cascade of events could lead to an acute
coronary syndrome (ie: acute MI)

Coronary Circulation
 Coronary arteries and veins
 Myocardium extracts the largest amount of
oxygen as blood moves into general
circulation
 Oxygen uptake by the myocardium can
only improve by increasing blood flow
through the coronary arteries
 If the coronary arteries are blocked, they
must be reopened if circulation is going to
be restored to that area of tissue supplied

12-Lead Electrodes
 A lead is a tracing of the electrical activity
between 2 electrodes
 Leads view the heart from the front of the body
 Top, bottom, right, and left side of heart
 Leads view the heart as if it were sliced in half
horizontally
 Front, back, right, and left sides of heart
 Each lead has a positive and a negative
electrode

Standard 12-Lead EKG
 Six limb leads
 Leads I, II, III, aVR, aVL, aVF
 Six chest leads (precordial leads)
 V1, V2, V3, V4, V5, V6
 Information from 12 leads obtained
from the attachment of only 10
electrodes

View The Leads Provide
 II, III, aVF – view inferior wall of heart
 V1 and V2 – view septal wall of heart
 V3 and V4 – view anterior wall of
heart
 I, aVL, V5, V6 – view lateral wall of
heart

Preparation for 12 Lead EKG
 Skin preparation
 Hair removal
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 spray

 Patient positioning
 Preferably flat
Heart rotates position as the patient
position changes
 If patient is elevated, note that
information on the EKG

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
V5 - 5th intercostal space, anterior axillary line
V6 - 5th intercostal space, mid-axillary line

 Precordial
leads
2nd ICS
1st ICS
3rd ICS

12 Lead EKG Printout
 Standard format 81/2 x 11 paper
 12 lead format:
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Machines can analyze data obtained
but humans must interpret data

I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6

Lateral View – I, aVL, V5, V6
I
aVL
V5
V6

Inferior View – II, III, aVF
II
III aVF

Anterior View – V3 & V4
V4
V3

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; damage
permanent; may have Q wave

Why A Pre-hospital EKG?
 EMS looking for ST segment elevation
 Indicates injury that can be reversible if found
early and acted upon early
 TIME IS MUSCLE
 The earlier the discovery of an acute cardiac
event, the quicker the patient can receive the
most appropriate care
 EKG’s sent to the ED before patient arrival
allows for the right personnel to be available to
properly care for the patient in the most time
efficient manner

What Does EMS Have to Do?
 Obtain a 12 lead EKG
 EMS to evaluate the leads as they are
sending the 12 lead to the ED
 Identify for the presence or absence of ST
elevation
 EMS to report what they see, not just what
is printed on the machine copy of the EKG
 Upon arrival, EMS to hand a copy of their
12 lead to the ED staff while they give
bedside report

Evaluating for ST Segment
Elevation
 Locate the J-point
 Identify/estimate where the isoelectric line
is noted to be
 Compare the level of the ST segment to
the isoelectric line
 Elevation (or depression) is significant if
more than 1 mm (one small box) is seen in
2 or more leads facing the same
anatomical area of the heart
(ie: contiguous leads-see slide #41, #42)

 J point – where the QRS complex and ST
segment meet
 ST segment elevation - evaluated 0.04 seconds
(one small box) after J point
The J Point

 Coved
shape
usually
indicates
acute injury
 Concave
shape is
usually
benign
especially if
patient is
asympto-
matic

Significant ST Elevation
 ST segment elevation measurement
 starts 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 (ie: II, III, aVF; I, aVL, V5, V6)
 Contiguous lead
 limb leads that “look” at the same area of the
heart or are numerically consecutive chest
leads (ie: V1 – V6)

Contiguous Leads
 Lateral wall: I, aVL, V5, V6
 Inferior wall: II, III, avF
 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)

Evolution of AMI
A - pre-infarct (normal)
B - Tall T wave (first few
minutes of infarct)
C - Tall T wave and ST
elevation (injury)
D - Elevated ST (injury),
inverted T wave (ischemia),
Q wave (tissue death)
E - Inverted T wave
(ischemia), Q wave (tissue
death)
F - Q wave (permanent
marking)

EKG monitoring
 Evaluates electrical activity of the heart
 Can indicate myocardial insult and location
ischemia - initial insult; ST depression seen
injury - prolonged myocardial hypoxia or
ischemia; ST elevation seen
infarction - tissue death
 dead tissue no longer contracts
 amount of dead tissue directly relates to
degree of muscle impairment
 may show Q waves

Contiguous ECG Leads
 EKG changes are
significant when they
are seen in at least
two contiguous leads
 Two leads are
contiguous if they
look at the same area
of the heart or they
are numerically
consecutive chest
leads

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

Basic 12-Lead EKG Format
Lead I
Lateral wall
aVR
not evaluated
V1
Septum
V4
Anterior wall
Lead II
Inferior wall
aVL
Lateral wall
V2
Septum
V5
Lateral wall
Lead III
Inferior wall
aVF
Inferior wall
V3
Anterior
V6
Lateral wall

Lateral Wall MI: I, aVL, V5, V6
Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.

Inferior Wall MI II, III, aVF

Septal MI: Leads V1 and V2

Anterior Wall MI V3, V4

Posterior MI – Reciprocal Changes
ST Depression V1, V2, V3, poss V4

Complications of Lateral Wall MI
 I, aVL, V5,V6
 Complications arise due to the conduction
components that are in the septum
 Conduction dysrhythmias most common
 Second degree Type II – classical
 3rd degree – complete heart block
 Bundle branch blocks
 Monitor patient closely for these blocks
 2nd degree Type II and 3rd degree are serious
dysrhythmias that need to be treated aggressively
with TCP

Complications of Inferior Wall MI
 II, III, aVF
 40% of patients with inferior MI’s have right
ventricular infarcts
 In the presence of a right ventricular infarct, there is a
high likeliness of both ventricles being damaged
 Contraction capabilities will be negatively affected
 Patients may present hypotensive
 Nitrates and Morphine alone will dilate blood vessels
worsening hypotension
 Under Medical Control direction patients are often
treated with a fluid challenge with the nitrates
 1st degree heart block and Second degree Type I
Wenckebach most common heart blocks

Complications of Septal Wall MI
 V1 and V2
 Significant amount of conduction components
are in the septal area
 Patient predisposed to dysrhythmia
 Second degree Type II – classical
 3rd degree heart block
 Bundle branch block
 Lethal heart blocks treated aggressively - TCP
 Rare to have a septal MI alone
 Common to have anterior or lateral involvement along
with septal area

Complications of Anterior Wall MI
 V3, V4
 Known as the “widowmaker” due to the potential
for a massive area of infarction from blockage of
the large amount of myocardium supplied by the
LAD (left anterior descending artery)
 Often the septal or lateral walls are also involved
 Watch for lethal ventricular dysrhythmias and
cardiogenic shock
 Second degree Type II and 3rd degree heart
block are more common than other blocks

Anterior Wall MI - V3, V4
 Early death within a few days often from CHF
 Massive area of ventricular tissue infarcted if LAD
totally occluded
 Important to obtain history of recent MI
diagnosis and hospital discharge
 Increased incidence of ventricular tachycardia
(VT) and ventricular fibrillation (VF) up to 1 -2
weeks post acute anterior MI

Additional Complications
 Acute pulmonary edema
 Nitroglycerin given to dilate blood vessels and
reduce preload
 Lasix given to dilate blood vessels and reduce
preload; as a diuretic
 Morphine given to dilate blood vessels and
reduce preload; reduce anxiety
 All medications and interventions (ie:
CPAP) can drop the B/P – monitor
carefully

Additional Complications
 Cardiogenic shock
 Ineffective pumping from the damaged heart
 IV fluid challenge if lung sounds are clear
 Dopamine drip titrated to maintain a systolic blood
pressure of >100 mmHg
Start at a low dose (5mcg/kg/min)
 Estimate the patient’s pounds (ie: 100 #)
 Take the 1st 2 numbers dropping the last
number (“10”)
 Minus 2 from the 1st 2 numbers
 This is the starting point for minidrips/minute
(10 – 2 = 8 minidrips/minute)

Common Terms Patients
Use To Describe Chest Pain
Heaviness
Pressing
Suffocating
Squeezing
Strangling
Burning
Constricting band
A weight in the
center of my chest
A vise tightening
around my chest

Additional Patient Complaints or
Presentations
Difficulty breathing
Excessive sweating
Unexplained nausea
or vomiting
Generalized
weakness
Dizziness
Syncope or near-
syncope
Palpitations
Isolated arm or jaw
pain
Fatigue
Dysrhythmias

Typical Injury Patterns

Atypical Presentation in the Elderly
 Most frequent symptoms of acute MI:
 Shortness of breath
 Fatigue and weakness (“I just don’t feel well”)
 Abdominal or epigastric discomfort
 Often have preexisting conditions making this
an already vulnerable population
 Hypertension
 CHF
 Previous AMI
 Likely to delay seeking treatment

Atypical Presentation in Women
 Discomfort described as:
 Aching
 Tightness
 Pressure
 Sharpness
 Burning
 Fullness
 Tingling
Often have no actual chest pain to offer as a
complaint. Often the pain is in the back,
shoulders, or neck
 Frequent acute
symptoms:
 Shortness of breath
 Weakness
 Unusual fatigue
 Cold sweats
 Dizziness
 Nausea/vomiting

Atypical Presentation in the
Patient With Diabetes
 Atypical presentation due to autonomic
dysfunction
 Common signs/symptoms:
 Generalized weakness
 Generalized feeling of not being well
 Syncope
 Lightheadedness
 Change in mental status

Region X SOP – Acute Coronary
Syndrome
 A 12 lead EKG is obtained on all patients
presenting with signs and symptoms of
acute MI
OR
 For patients where suspicions are raised
that the patient may be experiencing an
acute MI (ie: heart block)

Region X SOP – Acute Coronary
Syndrome
 Determine if the patient is stable or
unstable to proceed with interventions
 Easiest way to determine stability is to
evaluate blood flow
 What is the level of consciousness?
 What is the blood pressure / is there a radial
pulse?
 Remember: A B/P reading of 100/systolic
does not necessarily indicate the presence
or absence of symptoms

Oxygen
 In the presence of an acute MI, the
myocardium is being deprived of blood
flow and therefore adequate oxygen levels
 Provide what the patient needs
 Evaluate each individual clinical
presentation
 All patients deserve some form of oxygen
in this early period of myocardial starvation
for it

Aspirin
 Used to prevent platelet aggregation
 When a plague ruptures, chemicals are released.
Platelets congregate to the area to seal the rupture.
Platelet aggregation further increases the degree of
vessel blockage.
 Field dosage is 4 – 81 mg (324 mg total) baby
aspirin chewed
 Chewing breaks down the aspirin and allows for
faster absorption
 Give dose if patient not reliable about taking
their own dose or has not taken any aspirin

Nitroglycerin
 Venodilator
 Improves coronary blood flow
 By dilating blood vessels, pools blood away
from the heart which decreases preload. This
decreases the work load of a stressed heart.
 Carefully monitor blood pressure before and
after dosages
 Field dosage is 0.4 mg tablet sl
 Dosage can be repeated in 5 minutes if blood
pressure remains stable
 FYI: Pain level will not drop to “0” until the clot
is removed

For CMC EMS System Participants
 If the patient is <35 years of age
 Follow Acute coronary Syndrome SOP by
administering aspirin
 Medical Control contacted prior to
administration of nitroglycerin or morphine
 There should be no delay in obtaining a 12 lead
EKG in the field and transmitting it to the ED
 A visual interpretation is to be given during
report to the receiving hospital even when the 12
lead EKG is faxed in

Morphine
 CNS depressant to reduce anxiety
 Venodilates blood vessels to reduce the
volume of blood returning to the heart to
decrease the heart’s workload
 Field dosage is 2 mg slow IVP
 Dosage started when the 2nd dose of
nitroglycerin proves ineffective
 Dosage may be repeated every 2 minutes as
needed
 Maximum dosage is 10 mg
 Watch for hypotension

Receiving Hospital Report
 When sending a 12 lead EKG, EMS to
inform the receiving hospital what
identifiers have been used
 Department ID number
 Patient sex (M / F)
 Patient age
 Any other identifier
 EMS should always give their visual
interpretation of what they have observed
for ST elevation

Activating a Cardiac Alert
 The ED activates a cardiac alert to prepare the
cardiac team to provide optimal care for the
patient
 Typical cardiac alert team members
 ED staff – MD, RN, tech, secretary
 Cardiologist
 Cath lab personnel
 EKG tech (may be an ED staff member)
 Lab tech
 X-ray tech
 Not all hospitals use all members in a formalized
team but all of these members are somehow
integrated into the care of the patient

When Does a Cardiac Alert Get
Called?
 When EMS sends a 12 lead EKG with ST
elevation, the team gets activated
 When EMS confirms what they see on the
12 lead, whether the EKG is sent or not,
may trigger a cardiac alert
 There is a direct link in EMS accuracy,
completeness in patient report, and EKG
interpretation with pre-hospital activation
of the cardiac alert team

Transferring Care of The Patient to
The ED
 Bedside report is restated to the ED
personnel in the room
 The main report must be to an RN or MD
 Rhythm strips and 12 lead EKG are
presented
 Important to note positive and negative
changes in the patient condition
 Pain level has decreased
 Blood pressure has dropped

EKG Practice
 Practice reviewing the following 12 lead
EKG’s for ST segment elevation
 Evaluate the ST segment at the J point
 Note: A peaked T wave is not equivalent
with ST elevation
 Consider potential complications to
monitor for based on the location of the
acute MI
 Vignette follows the 12 lead EKG picture

Practice Identifying ST Segment
Elevation
> 1mm (1 small box) above the baseline 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

Case #1
 52 year-old patient complains of
indigestion after pizza & beer dinner.
 VS: 124/82; P – 108; R - 18
 Is there ST elevation:
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 What are you going to do for this patient?
 (There is no ST elevation)

Case #2
 62 year-old female developed chest & jaw pain
while in the shower
 VS: 110/62; P – 66; R – 20
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (ST elevation II, III, aVF – Inferior wall MI)

Case #3
 45 year-old patient who complains of chest
heaviness & lightheadedness
 VS: 90/56; P – 86; R - 22
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (ST elevation V2-V5 – anterior infarction)

Case #4
 87 year-old female patient complains of
dizziness and being extremely tired
 VS: 88/52; P – 30; R - 16
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (ST elevation II, III, aVF, V2-V4)

Case #5
 58 year-old male patient who complains of chest
pain radiating down the left arm after working
out in the gym
 VS: 110/72; P – 100; R - 18
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (ST elevation II, III, aVF)

Case #6
 92 year-old patient complaining of pounding in
her chest for one hour
 VS: 98/66; P – 110; R- 16
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (ST elevation V1-V4 – anterioseptal MI)

Case #7
 66 year-old patient with history of diabetes
for 25 years complains of being
lightheaded and is sweaty
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (Normal EKG – sinus bradycardia)

Case #8
 70 year-old patient had a syncopal episode
when they stood up from the couch
 VS: 156/98; P – 76; R - 16
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (ST elevation V2, V3, slightly in V1, V4)

Case #9
 82 year-old patient complains of sudden onset of
slurred speech, inability to grasp a coffee cup,
and inability to follow simple commands
 VS: 122/84; P – 110; R - 18
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (No ST elevation, atrial fibrillation rhythm)

Case #10
 36 year-old patient who passed out standing in
line at a bank
 VS: 128/78; P – 80; R - 20
 I, aVL, V5, V6?
 II, III, aVF?
 V1, V2?
 V3, V4?
 (ST elevation II, III, aVF)

Bibliography
 Aehlert, B. EKG’s Made Easy third Edition.
Elsevier Mosby. 2006.
 Beasley, B. Understanding EKG’s A
Practical Approach. Brady. 2003.
 Bledsoe, B., Porter, R., Cherry, R.
Paramedic Care Principles and Practices.
Third Edition. Brady. 2009.
 Ellis, K. EKG Plain and Simple. Prentice
Hall. 2002.
 Page, B. 12 Lead EKG for Acute and
Critical Care Providers. Brady. 2005.

 Phalen, T., Aehlert, B. The 12 Lead EKG in
Acute Coronary Syndromes. Second Edition,
Elsevier Mosby. 2006.
 Region X SOP’s. March 2007, Amended
January 1, 2008.
 freemd.com (Acute Coronary Syndrome 9/2008)
 www.anaesthetist.com/icu/organs/heart/ecg/Find
ex.htm
 www.ecglibrary.com/
 www.gwc.maricopa.edu/class/bio202/cyberheart
/ekgqzr.htm
 www.madsci.com/manu/ekg_mi.htm

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