Download 12 Lead ECG

9/28/2016
12 Lead ECG – The Basics
Dawn Gosnell, MSN, APRN-CNS, CCRN
October 2015
1
Agenda
Over two hours with a small break
 ECG Interpretation Tools
o
o
o
o
o
o
Lead placement
Coronary Arteries
3 I’s of an MI
Bundle Branch Blocks
Axis Deviation
VT vs. SVT with a Wide QRS
 AMI Clinical Practice Guidelines
 12 Lead ECG Practice
2
Objectives
1. Identifies ECG changes associated with
myocardial ischemia, injury, and
infarction.
2. Associates lead views with the
correlating area of the heart.
3. Selects appropriate clinical practice
guidelines for the acute myocardial
infarction patient, including anti-platelet,
beta blocker, and statin therapies.
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Lead Placement Matters
•
•
Up to 50% of cases have the V1 and V2
electrodes above the 4th intercostal
location, which can mimic an anterior MI
and cause T wave inversion.
Up to 33% of cases have the precordial electrodes
misplaced, which can alter the amplitude and lead
to a misdiagnosis.
V1
V2
V3
V4
V5
V6
RL
RA
LL
LA
4th intercostal space to the right of the
sternum
4th intercostal space to the left of the
sternum
Midway between V2 and V4
5th intercostal space at the
midclavicular line
Anterior axillary line at the same level
as V4
Midaxillary line at the same level as
V4 and V5
Anywhere above the ankle and below
the torso - right
Anywhere between the shoulder and
elbow – right
Anywhere above the ankle and below
the torso – left
Anywhere between the shoulder and
the elbow – left
Bipolar Limb Leads
Einthovens triangle
Lead I
 Measures electrical
potential between right arm
(-) and left arm (+).
Lead II
 Measures electrical
potential between right arm
(-) and left leg (+).
Lead III
 Measures electrical
potential between left arm
(-) and left leg (+).
Unipolar Limb Leads
avR – right arm (+)
avL – left arm (+)
avF – left foot (+)
Right foot is a ground lead
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Precordial or Chest Leads
Right Sided ECG
May be useful in the
diagnosis of a right
ventricular infarct.
19-51% of inferior
MIs
or Left Main
or Obtuse Marginal
Some patients
have an additional
coronary artery off
the left main
called the ramus
or intermediate
artery.
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Right Coronary Artery
(RCA)
SA node – 55% people
AV node, bundle of His –
90% people
Right atrium
Inferior left ventricle
Lower 1/3 of septum
Major portion anterior right
ventricle and posterior right
ventricle
Posterior left ventricle
papillary muscles
Posterior division left bundle
branch
Circumflex
(Cx)
SA node – 45%
people
AV node – 10%
people
Lateral and
posterior left
ventricle
Posterior left
bundle branch
Left atrium
Left Coronary Artery
(LCA,LAD)
Anterior 2/3rds of
septum, bundle
branches
Left ventricle –
anterior, apex,
posterior)
Minor portion of right
ventricle
(Conover, 2003)
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Steps to Interpreting the ECG
Basic rhythm steps
Rhythm
Rate
P Waves
PR Interval
QRS
Additional 12 Lead steps
Wall of the heart
What’s abnormal with each
lead
3 I’s of a MI
Axis
Bundle Branch Blocks
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An electrocardiography pearl
ECG is nothing more than a voltmeter and
a stopwatch.
 Timing
 Voltage


Scars decrease the voltage.
Thick muscle increases the voltage.
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What is Normal in the 12 Lead
12 Lead Format
1
AVR
V1
V4
2
AVL
V2
V5
3
AVF
V3
V6
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Wall
Leads
Coronary Artery
Reciprocal
changes
Anterior
V1, V2, V3, V4
LAD branch of LCA
II, III, aVF
Inferior
II, III, aVF
RCA
I, aVL
Lateral
I, aVL, V5, V6
Circumflex branch of
LCA
V1, V3
V1, V2
RCA, Circumflex
Posterior
(ST depression, tall
R waves)
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Apical
V3, V4, V5, V6
LAD, RCA
Anteriolateral
I, aVL, V1, V2,
V3, V4, V5, V6
LAD, Circumflex
Septal
V1, V2
LAD
II, III, aVF
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3 I’s of a MI
Injury
 ST elevation on the affected side
Infarction
 Significant Q waves
Ischemia
 Inverted T waves
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Injury
ST Elevation
General guidelines:
>1 mm in limb leads
> 2 mm in chest leads
Acute injury is occurring. Heart attack is happening now.
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Causes of ST Elevation
Acute MI
Injury pattern
Left BBB
Angina with coronary artery
spasm
Early repolarization
Left Ventricular hypertrophy
Hyperkalemia
Infarction
Tako Tsubo cardiomyopathy
Intracranial bleeds or other
pathologies like tumors
Acute corpulmonale
Myocarditis
Pericarditis
Cholecystitis
Myocardial tumors
Acute pancreatitis
Hypothermia
Significant Q Waves
Q waves develop over
4 to 24 hours and remain
for life.
Significant Q waves are 25-33% of the R wave.
Q > 0.038 seconds
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Q-Waves
Physiologic
Pathologic
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Ischemia
Inverted T waves
Supply and Demand problem.
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Acute
Chronic
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Signs and Symptoms of Acute
Coronary Syndrome
Classic or usual





Chest discomfort described as pain,
pressure, ache, squeezing, burning or
fullness.
Discomfort or pain in one or both arms
Shortness of breath with or before
chest discomfort
Diaphoresis - sweating
Anxiety
Atypical or not usual





Back, abdominal, neck or jaw pain
Weakness or fatigue
Indigestion
Nausea or vomiting
Dizziness or lightheadedness
Prodromal symptoms or pre-heart attack
symptoms can occur one to six weeks before include:
Chest pain
Pain in one shoulder blade or upper back
Indigestion
Unusual fatigue
Anxiety
Sleep disturbances
Shortness of breath, especially if no
previous awareness of heart disease
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Acute Coronary Syndrome
 ST Elevated Myocardial Infarction


STEMI or new LBBB
Classic presentation with elevated cardiac biomarkers
 Non ST Elevated Myocardial Infarction
NSTEMI
ST and T-wave changes with elevated cardiac
biomarkers
 Classical or atypical presentation


 Angina, Unstable angina
Types of MI
Type 1
Type 3
•
•
•
Spontaneous MI related to ischemia due
to a primary coronary event such as
plaque erosion and/or rupture, fissuring,
or dissection.
Non ST Elevation MI or ST Elevation MI
Type 2
•
MI secondary to ischemia due to either
increased oxygen demand or decreased
supply.
o Coronary artery spasm, coronary
embolism, anemia, arrhythmias,
hypertension, or hypotension
o Respiratory distress, renal failure,
sepsis
•
•
Sudden unexpected cardiac death,
including cardiac arrest, often with
symptoms suggestive of MI.
Accompanied by presumably new ST
elevation or new LBBB
Evidence of fresh thrombus in the
coronary artery by angiography
Type 4
•
MI associated with coronary angioplasty
or stent.
Type 5
•
MI associated with coronary artery
bypass grafting (CABG)
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Pathological Types
Transmural AMI
•
•
•
•
Infarct extends through the whole thickness of the heart muscle, usually
resulting in complete occlusion of the area’s blood supply.
Associated with atherosclerosis involving a major coronary artery.
Subclassified into anterior, posterior, inferior, lateral, or septal.
ST elevation, and Q-waves
Subendocardial AMI
•
•
•
Involves a small area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles.
Susceptible to ischemia.
ST depression, T-wave changes
AMI Clinical Practice Guidelines (CPGs)
During hospitalization
 Reperfusion strategies
 Aspirin within 24 hours before or after arrival
 Smoking (tobacco) cessation advice/counseling
At Discharge
 Aspirin
 Beta-Blocker
 Statin
 ACE-I or ARB therapy for left ventricular systolic
dysfunction, EF (ejection fraction) < 40%
STEMI Reperfusion Strategy
Door-to-needle goal of 30 minutes Thrombolytic
(fibrinolysis) therapy
 TNKase (tenecteplase)
 Activase (t-PA, alteplase)
 Retavase (r-PA, reteplase)
 Streptokinase (Streptase)
Door-to-Balloon (D2B) within 90 minutes
 Angioplasty
PTCA – Percutaneous Transluminal Coronary
Angioplasty
 Coronary artery stents
 Atherectomy Percutaneous Coronary Intervention

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Transradial Approach
TR Band
•
•
With PCI – on for 90 minutes,
then 2 mLs every 15 minutes
Without PCI – on for 60
minutes, then 2 mLs every
15 minutes
If bleeding occurs, re-inflate
the 2 mLs, wait 30 minutes, then
resume removal process.
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Percutaneous Coronary
Intervention - PCI
 Angioplasty
 Atherectomy
 Coronary stenting
Bare metal (BMS)
Drug eluting (DES)
 Bioresorbable (BVS)


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BVS – Bioresorbable coronary
stents
Abbott Absorb III
• Thicker like 1st
generation metal
stents
• Candidate selection
 Vessel > 2.5 mm
• Technique will be
important
• Won’t see stent, only
the markers
https://www.absorb.com/mechanism-ofaction?gclid=CLnK79DBoc8CFUM2gQodT
WsKJQ
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Closure Devices
 Angio-Seal
 Mynx
 Perclose
 Closure Pads
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Antiplatelet Therapy
Aspirin
• 162 to 325 mg initially
• 81 to 325 mg daily
Duration of Dual
Antiplatelet Therapy
New 2016 guidelines
• http://circ.ahajournals.o
rg/content/134/10/e123
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Antiplatelet & Anticoagulant Options
Name
Classification
Dosing
Comments
Peak effect – 1-3 hours
Aspirin
Anti-platelet, attaches to TXA2
site
81-325 mg PO per day
Plavix (clopidogrel)
Anti-platelet, attaches to ADP
P2Y12 site
300-600 mg PO loading, then 75 mg
daily
Effient (prasugrel)
Anti-platelet, attaches to ADP
P2Y12 site
60 mg PO loading, then 10 mg daily
Brilinta (ticagrelor)
Anti-platelet, attaches to ADP
P2Y12 site
180 mg PO loading, then 90 mg twice a
day
Peak effect – 2 hours after load
Hold 5 days
ASA to be limited to 75-100 mg/day
Integrilin (eptifibatide)
Anti-platelet, attaches to GP
IIb IIIa
2 mcg/kg/min infusion 12 to 24 hours
after PCI
-Decrease to 1 mcg/kg/min for renal
impairment
Reversible in 2.5-4 hours.
Don’t get patients OOB until 2-2.5
hours after infusion is shut off.
Angiomax (bivalirudin)
Anticoagulant
Direct thrombin (Factor II)
inhibitor
1.75 mg/kg/hr infusion started in HCL
and run up to 4 hours post procedure.
Consider reduction to 1 mg/kg/hr for
renal impairment.
No antidote or reversal agent.
Coagulation returns to baseline ~1
hour after discontinuation.
Half-life – 25 minutes
Heparin
Anticoagulant
Inhibits thrombin (Factor II)
and Factor X
Boluses of 5,000 – 10,000 units given
during the procedure.
Protamine ins the reversal agent.
Hold – 7 days optional
Peak effect – 6 hours after load
Hold – 5-7 days
Do not take with PPI, especially
Prilosec.
Peak effect – 4 hours after load
Hold 7 days
Caution in patients > 75 years old, <
60 kg, or history of stroke or TIA.
Beta Blockers
• Reduce catecholamine
levels
• Decrease myocardial
ischemia and limit infarct
size
• Reduce myocardial
workload and oxygen
demand
• Reduce heart rate and
blood pressure
• Reduce supraventricular
and malignant ventricular
arrhythmias
Metoprolol – Lopressor,
Toprol XL
Carvedilol – Coreg
Bisoprolol - Zebeta
Atenolol – Tenormin
Sotalol – Betapace
Betaxolol – Kerlone
Propranolol – Inderol
Esmolol – Brevibloc (IV)
Labetalol – Normodyne (IV)
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HMG-CoA Reductase
Cholesterol is synthesized
in the smooth
endoplasmic reticulum by
a series of chemical
reactions.
The first way to block
cholesterol synthesis is to
interrupt the conversion of
HMG CoA to mevalonate.
HMG-CoA Reductase Inhibitors or
Statins
2013 guideline update
•
Lifestyle modification
•
•
•
Diet, exercise, lose weight
Assess ASCVD risk
Four Benefit Groups
•
•
•
•
Individuals with clinical ASCVD
Individuals with primary elevations
of LDL-C >190 mg/dL
Individuals age 40-75 with diabetes
and LDL-C of 70-189 mg/dL without
clinical ASCVD
Individuals without clinical ASCVD
or diabetes who are age 40-75 with
LDL-C of 70-189 mg/dL and
estimated 10 year ASCVD risk of
>7.5%
Atorvastatin – Lipitor
Rosuvastatin – Crestor
Simvastatin – Zocor
Pravastatin – Pravachol
Lovastatin – Mevacor
Guidelines level to high or moderate
intensity dosing.
Adverse effects – muscle aching,
increase in liver enzymes
http://content.onlinejacc.org/article.aspx?articleid
=1879710
Moderate-Intensity
High-Intensity
Daily dose lowers LDL-C,
on average, by approximately >50%
• Atorvastatin (40) – 80 mg
• Rosuvastatin 20 – (40) mg
Daily dose lowers LDL-C, on average,
by approximately 30% to <50%
• Atorvastatin 10 (20) mg
• Rosuvastatin (5) 10 mg
• Simvastatin 20-40 mg
• Pravastatin 40 (80) mg
• Lovastatin 40 mg
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Hyperlipidemia
Alirucumab (Praluent)
• 70% of elevated LDL related to genetics
•
Praluent is an antibody that targets a specific protein, called PCSK9,
which works by reducing the number of receptors on the liver that
remove LDL cholesterol from the blood. By blocking PCSK9’s ability to
work, more receptors are available to get rid of LDL cholesterol from
the blood and, as a result, lower LDL cholesterol levels
• 75 mg or 150 mg SQ every 2 weeks
• No affect to liver.
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Renin-Angiotensin-Aldosterone
System
ACE-I & ARBs
ACE-I
Lisinopril – Prinivil, Zestril
Benazepril – Lotensin
Captopril – Capoten
Ramipril - Altace
Enalapril – Vasotec
Fosinopril – Monopril
Adverse effect – cough,
angioedema, hyperkalemia
Watch renal function.
ARB
Losartan – Cozaar
Valsartan - Diovan
Irbesartan – Avapro
Tend not to have as many
adverse effects. Cough
not really seen.
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http://content.onlinejacc.org/article.aspx?articleid=1486
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Patient Safety Indicators
Outcomes used for Hospital Value Based
Purchasing Measures
 30 day Mortality
 30 day Readmission
 Patient Experience of Care – HCAHPS
(Hospital Consumer Assessment of
Healthcare Providers and Systems Survey),
also know as Patient Satisfaction scores.
Coming in the Future
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Cardiac Bundling
Right versus Left BBB
RBBB - Right Bundle Branch Block
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QRS 162 ms
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RBBB
Right BBB is blocked.
 Electrical impulse is going Left
Physiological
 Athletes

> Right
An incomplete BBB measures
< 0.12 sec
Increased muscle mass
Pathological




CAD
Pulmonary HTN
Inflammatory disease
Lesions of the septum
 New RBBB after bypass
surgery is a + periop MI
LBBB - Left Bundle Branch Block
53
QRS 144 ms
LBBB
Left BBB is blocked
 Electrical impulse is going
Right > Left
LBBB receives blood from
left and right coronary
arteries.
Left bundle of HIS has 3
fascicles (fascicular block)
Pathological





CAD
Hypertension
Dilated cardiomyopathy
Calcified aortic valve
Degenerative heart disease
 Anterior (superior)
 Posterior (inferior)
 Midseptum
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Determining Axis
Axis
Axis
Lead I
Lead II
Lead III
Comments
Normal
0-90
aVF positive
Physiologic
Left Axis
0--40
aVF negative
Pathological
Left Axis
-40 to -90
Anterior
Hemiblock
Right Axis
90-180
aVF positive
Posterior
Hemiblock
Extreme Right
Axis
No Man’s Land
aVF negative
Ventricular in
origin
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Some physiological normal
found
 0 to -30 (-40)
 +90 to +120
O to +90
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Physiological




Too short, Too tall
Obese
Older
Pregnant
Pathological






0 to –90
Left Ventricular Hypertrophy
Hyperkalemia
Qs in Inferior Mi
Anterior hemiblock
Left BBB
WPW w/ Right sided access
pathway
 Emphysema
Physiological
 Normal in children and thin
adults
Pathological







Right Ventricular Hypertrophy
Anterior-Lateral MI
Posterior hemiblock
Right BBB
COPD w/o Pulmonary HTN
Pulmonary Emboli
WPW w/ Left sided accessory
pathway
 ASD, VSD
+90 to +180
No Man’s Land
Ventricular Tachycardia
Ventricular Pacing
Hyperkalemia
Emphysema
+180 to -90
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Brugada Criteria for Ventricular Tach
1.
2.
3.
4.
5.
Is there extreme right axis?
Is there an RS complex?
Is the QRS wide?
Is there AV Dissociation?
Is there concordance in V1-V6?
Spread the Message
Golden
Hour
References
Amsterdam, E. A., Wenger, N. K., Brindis, R. G., Casey, D. E. Ganiats, T. G.,
Holmes, D. R, …Zieman, S. J. (2014). 2014 AHA/ACC guideline for the
management of patients with non-st-elevation acute coronary syndromes.
Retrieved from http://content.onlinejacc.org/article.aspx?articleid=1910086
Levine, G. N., Bates, E. R., Bittl, J. A., Brindis, R. G., Fihn, S. D., Fleisher, L. A.,
…Smith, S. C. (2016). 2016 ACC/AHA guideline focused update on duration of
dual antiplatelet therapy in patients with coronary artery disease. Retrieved from
http://circ.ahajournals.org/content/134/10/e123
O’Gara, P. T., Kushner, F. G., Ascheim, D. D., Casey, D. E., Chung, M. K., de
Lemos, J. A., …Zhao, D.X. (2013). 2013 ACCF/AHA guideline for the
management of st-elevation myocardial infarction. Circulation, 127. Retrieved
from
http://circ.ahajournals.org/content/early/2012/12/17/CIR.0b013e3182742cf6.full.p
df+html
Shenasa, M., Josephson, M. E., & Mark Estes, N. A. (2015). ECG handbook of
contemporary challenges. Minneapolis, MN: Cardiotest Publishing.
Thaler, M. S. (2015). The only ecg book you’ll ever need (8th ed.). Philadelphia, PA:
63 Wolters Kluwer Health.
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