9/28/2016

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12 Lead ECG – The Basics

Dawn Gosnell, MSN, APRN-CNS, CCRN

1October 2015

Agenda

Over two hours with a small break

ECG Interpretation Toolso Lead placement

o Coronary Arteries

o 3 I’s of an MI

o Bundle Branch Blocks

o Axis Deviation

o 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

V1 4th intercostal space to the right of the

sternum

V2 4th intercostal space to the left of the

sternum

V3 Midway between V2 and V4

V4 5th intercostal space at the

midclavicular line

V5 Anterior axillary line at the same level

as V4

V6 Midaxillary line at the same level as

V4 and V5

RL Anywhere above the ankle and below

the torso - right

RA Anywhere between the shoulder and

elbow – right

LL Anywhere above the ankle and below

the torso – left

LA Anywhere between the shoulder and

the elbow – left

• 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.

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

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or Obtuse Marginal

Some patients have an additional coronary artery off

the left main called the ramus or intermediate

artery.

or Left Main

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Right Coronary Artery

(RCA)

Circumflex

(Cx)

Left Coronary Artery

(LCA,LAD)

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

SA node – 45%

people

AV node – 10%

people

Lateral and

posterior left

ventricle

Posterior left

bundle branch

Left atrium

Anterior 2/3rds of

septum, bundle

branches

Left ventricle –

anterior, apex,

posterior)

Minor portion of right

ventricle

(Conover, 2003)

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

Posterior V1, V2

(ST depression, tall

R waves)

RCA, Circumflex

Apical V3, V4, V5, V6 LAD, RCA

Anteriolateral I, aVL, V1, V2,

V3, V4, V5, V6

LAD, Circumflex II, III, aVF

Septal V1, V2 LAD

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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

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Acute injury is occurring. Heart attack is happening now.

General guidelines:

>1 mm in limb leads

> 2 mm in chest leads

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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

Tako Tsubo cardiomyopathy

Intracranial bleeds or other

pathologies like tumors

Acute corpulmonale

Myocarditis

Pericarditis

Cholecystitis

Myocardial tumors

Acute pancreatitis

Hypothermia

Infarction Significant Q Waves

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Significant Q waves are 25-33% of the R wave.Q > 0.038 seconds

Q waves develop over4 to 24 hours and remainfor life.

Q-Waves

Physiologic Pathologic

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Ischemia Inverted T waves

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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

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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

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• 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

Type 3• 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

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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.

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-of-

action?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

Aspirin Anti-platelet, attaches to TXA2

site

81-325 mg PO per day Peak effect – 1-3 hours

Hold – 7 days optional

Plavix (clopidogrel) Anti-platelet, attaches to ADP

P2Y12 site

300-600 mg PO loading, then 75 mg

daily

Peak effect – 6 hours after load

Hold – 5-7 days

Do not take with PPI, especially

Prilosec.

Effient (prasugrel) Anti-platelet, attaches to ADP

P2Y12 site

60 mg PO loading, then 10 mg daily Peak effect – 4 hours after load

Hold 7 days

Caution in patients > 75 years old, <

60 kg, or history of stroke or TIA.

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.

Beta Blockers

Metoprolol – Lopressor,

Toprol XL

Carvedilol – Coreg

Bisoprolol - Zebeta

Atenolol – Tenormin

Sotalol – Betapace

Betaxolol – Kerlone

Propranolol – Inderol

Esmolol – Brevibloc (IV)

Labetalol – Normodyne (IV)

• 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

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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

High-Intensity Daily dose lowers LDL-C,

on average, by approximately >50%

• Atorvastatin (40) – 80 mg

• Rosuvastatin 20 – (40) mg

Moderate-IntensityDaily 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

115

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

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RBBB - Right Bundle Branch Block

QRS 162 ms

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RBBB

Right BBB is blocked.

Electrical impulse is going Left

> Right

An incomplete BBB measures

< 0.12 sec

Physiological

Athletes

Increased muscle mass

Pathological

CAD

Pulmonary HTN

Inflammatory disease

Lesions of the septum

New RBBB after bypass

surgery is a + periop MI

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LBBB - Left Bundle Branch Block

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)

Anterior (superior)

Posterior (inferior)

Midseptum

Pathological CAD

Hypertension

Dilated cardiomyopathy

Calcified aortic valve

Degenerative heart disease

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Determining Axis

Axis

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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

O to +90

Some physiological normal

found 0 to -30 (-40)

+90 to +120

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0 to –90

Physiological Too short, Too tall

Obese

Older

Pregnant

Pathological Left Ventricular Hypertrophy

Hyperkalemia

Qs in Inferior Mi

Anterior hemiblock

Left BBB

WPW w/ Right sided access

pathway

Emphysema

+90 to +180

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

+180 to -90

No Man’s Land

Ventricular Tachycardia

Ventricular Pacing

Hyperkalemia

Emphysema

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Brugada Criteria for Ventricular Tach

1. Is there extreme right axis?

2. Is there an RS complex?

3. Is the QRS wide?

4. Is there AV Dissociation?

5. 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:

Wolters Kluwer Health.63