February 2009 12 Lead EKG
Download
Report
Transcript February 2009 12 Lead EKG
Overview of Revised
CMC EMS System CE;
12 Lead EKG’s
February 2009 CE
Site Code #107200E1209
Prepared by:
Bill Glade, DC Wauconda Fire Department
Sharon Hopkins, RN, BSN
Objectives
Upon successful completion of this module, the
EMS provider will be able to accomplish the
following:
Identify changes in the Advocate Condell EMS System
CE program as taught in class.
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 following
guidelines reviewed in class.
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
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
Actively participate in 12 lead EKG scenario practice
and discussion
Given a picture, correctly trace the order of the
cardiac conduction system.
Given a manikin, correctly place electrodes to obtain
a 12 lead EKG.
CMC EMS CE Process For 2009
Educational committee formed to develop a new
CE process that will be evolving
7 CE’s presented by EMS staff
2 CE’s presented by department members
Total of 27 hours of CE per year
Objectives and references for each CE sent to
departments for preview
Each department will receive a detailed copy of
the CE material for reference
CE power points will continue to be posted on
the Condell website
2009 CE Process
All CE’s must be completed by year’s end
Medical Officer will oversee the completion for
those not completing during EMS staff
presentation
There will no longer be biannual exams
Quizzes will be administered at the completion
of each CE
Successful completion is at 80%
Number of quiz questions may be variable dependent
on topic and will be based on objectives
Handouts at class will only be material
applicable to complete that topic and no longer
the full power points
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
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
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
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 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
1st ICS
2nd ICS
3rd ICS
12 Lead EKG Printout
Standard format 81/2 x 11 paper
12 lead format:
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Machines can analyze data obtained
but humans must interpret data
Lateral View – I, aVL, V5, V6
Inferior View – II, III, aVF
Septal View – V1 & V2
Anterior View – V3 & V4
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 Do You Have to Do?
Obtain a 12 lead EKG
Evaluate the leads yourself as you are
sending the 12 lead to the ED
Identify for the presence or absence of ST
elevation
Report what you see, not just what is
printed on the machine copy of the EKG
Upon arrival, hand a copy of your 12 lead
to the ED staff while you 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)
The J Point
J point – where the QRS complex and ST
segment meet
ST segment elevation - evaluated 0.04 seconds
(one small box) after J point
Coved
shape
usually
indicates
acute injury
Concave
shape is
usually
benign
especially if
patient is
asymptomatic
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
Contiguous lead
limb leads that “look” at the same area of the
heart or are numerically consecutive chest
leads
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)
ST Segment
Elevation
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
Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
Septal MI: Leads V1 and V2
Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
Anterior Wall MI V3, V4
Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
Posterior MI – Reciprocal Changes
ST Depression V1, V2, V3, poss V4
Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
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 to dilate blood vessels and
reduce preload
Lasix to dilate blood vessels and reduce
preload; as a diuretic
Morphine to dilate blood vessels and reduce
preload; reduce anxiety
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”)
This is the starting point for
minidrips/minute (8 minidrips/minute)
Common Terms Patients
Use To Describe Chest Pain
Heaviness
Burning
Pressing
Constricting band
Suffocating
A weight in the
center of my chest
Squeezing
Strangling
A vise tightening
around my chest
Additional Patient Complaints or
Presentations
Difficulty breathing
Excessive sweating
Unexplained nausea
or vomiting
Generalized
weakness
Dizziness
Syncope or nearsyncope
Palpitations
Isolated arm or jaw
pain
Fatigue
Dysrhythmias
Typical Injury Patterns
Source: The 12-Lead ECG in Acute Coronary Syndromes, MosbyJems, 2006.
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
Frequent acute
symptoms:
Shortness of breath
Weakness
Unusual fatigue
Cold sweats
Dizziness
Nausea/vomiting
Often have no actual chest pain to offer as a
complaint. Often the pain is in the back,
shoulders, or neck
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)
12-Lead Electrode Placement
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.
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
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
Contact Medical control 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
Your visual interpretation is to be given during
report to the receiving hospital
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
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, inform the
receiving hospital what identifiers have
been used
Department ID number
Patient sex (M / F)
Patient age
Any other identifier
Always give your visual interpretation of
what you 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 you send a 12 lead EKG with ST
elevation, the team gets activated
When you confirm what you see on the 12
lead, whether the EKG is sent or not, may
trigger a cardiac alert
There is a direct link in your 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
Documentation
Follow OPQRST guidelines
Some of this information is added into a check
box or other prompt; otherwise the information is
written into the narrative
Onset – what was the patient doing when the
problem/pain began? Any contributing factors?
Add this information to the narrative.
Provocation/palliation – what makes the pain
worse/makes it better; added to narrative
Quality- in the patient’s own words; added to
narrative
Region/Radiation – where is the problem/pain;
radiation is typically to the jaw, down an arm, felt
in the back; added to narrative
Severity – on a scale of 0-10, 0 being no pain
and 10 being the worse pain the patient has
experienced; use the “pain scale” box
Time – when did the problem/pain begin and
how long has it lasted? Use the “time of onset”
box.
Include associated symptoms like dyspnea or
nausea
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
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
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?
Case #2
Case #2
62 year-old female developed chest & jaw
pain while in the shower
VS: 110/62; P – 66; R – 20
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #3
Case #3
45 year-old patient who complains of chest
heaviness & lightheadedness
VS: 90/56; P – 86; R - 22
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #4
Case #4
87 year-old female patient complains of
dizziness and being extremely tired
VS: 88/52; P – 30; R - 16
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #5
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
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #6
Case #6
92 year-old patient complaining of
pounding in her chest for one hour
VS: 98/66; P – 110; R- 16
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #7
Case #7
66 year-old patient with history of diabetes
for 25 years complains of being
lightheaded and is sweaty
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #8
Case #8
70 year-old patient had a syncopal episode
when they stood up from the couch
VS: 156/98; P – 76; R - 16
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #9
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
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
Case #10
Case #10
36 year-old patient who passed out
standing in line at a bank
VS: 128/78; P – 80; R - 20
Is there ST elevation:
I, aVL, V5, V6?
II, III, aVF?
V1, V2?
V3, V4?
What are you going to do for this patient?
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