Chamberlain College of Nursing ECG Worksheet

Part I: Basic ECGStudent Learning Outcomes:
At the completion of part I, students will be able to:





Identify the parts of an ECG waveform and connect them to the corresponding events in the
heart
Measure waveform intervals and discriminate normal from abnormal intervals
Determine heartrate from an ECG tracing
Correctly identify common arrythmias
(note: students who work as nurses in areas where patients are routinely monitored and/or who
are ACLS certified, may already be competent in these areas and may elect to skip part 1. A note
of caution, however, if knowledge of the above is not solid, it will negatively affect the student’s
ability to progress successfully through the remainder of the module sections. The student may
self-assess and watch some or all of the videos depending on prior knowledge)
Readings:
Dubin, D. (2000). Rapid Interpretation of EKG’s, 6th ed. Fort Meyers, FL: COVER Publishing Company.
Chapters 1-6.
Activities:
1. Watch the following 4 part video series from ‘Films on Demand,’ entitled: EKG Interpretation and
Response Series.
It has 4 parts that should be watched in this order:




Reading an EKG: EKG interpretation and response (22min 31sec)
Sinus Dysrhythmias: EKG interpretation and response (13min 44 sec)
Atrial and Junctional Dysrhythmias and Heart Block: EKG interpretation and response (18:31)
Ventricular Dysrhythmias and Patient Care: EKG interpretation and response (13:34)
Links not working? Search “EKG Interpretation and Response” in the Films on Demand Database in
the Regis Library.
2. Practice rhythms with this online interactive activity: https://www.practicalclinicalskills.com/ekg
• Try the ‘EKG quiz’ and/or the ‘EKG tutor’ on this page
3. Describe your experience during the online activity.
Part 2: 12 Lead Basics
Objectives:
At the completion of part 2 the student will be able to:




Describe the basic principles of 12 lead ECG as a diagnostic tool
List the bipolar leads and delineate the areas of the heart for which they provide information
List the augmented voltage leads and delineate the areas of the heart for which they provide
information
List the augmented voltage leads and delineate the areas of the heart for which they provide
information
Readings:
Up to Date: “Basic Principles of Electrocardiographic Interpretation”
Dubin: Chapters 1 and 2
Activities:
1. Listen to the lecture capture of “12 lead basics”
2. Complete the related interactive exercise ’12 lead basics practice’ exercise
Part 3: Axis
Objectives:




Describe the concept of Axis
Differentiate among normal axis, right axis deviation, left axis deviation, and extreme axis
deviation
List causes of right and left axis deviation
Determine quadrant of axis by reviewing the ECG
Readings:
Dubin Chapter 7
Activities:
1. Listen to the lecture entitled ‘Axis’
2. Practice with an online interactive exercise:
https://ekg.academy/learn-ekg?courseid=322&seq=1
3. Describe your experience during the online activity.
Part 4: Hypertrophy
Objectives:
Define cardiac hypertrophy


List conditions that cause cardiac hypertrophy
Apply the criteria for determining cardiac hypertrophy by reviewing an ECG
Readings:
Up to Date: “Electrocardiographic diagnosis of left ventricular hypertrophy
Dubin, Chapter 8
Activities:
1. Listen to the lecture entitled “Hypertrophy”
2. Practice with an interactive online exercise:
https://ekg.academy/learn-ekg?courseid=321&seq=1
3. Describe your experience during the online activity.
Part 5: Ischemia, Injury, Infarction
Objectives:



Identify the ECG findings consistent with myocardial ischemia on an ECG
Identify the ECG findings consistent myocardial injury on an ECG
Identify the ECG findings consistent with myocardial infarction on ECG
Readings:
Up to Date: ‘ECG Tutorial: Myocardial ischemia and infarction’
Dubin, Chapter 9
Activities:
1. Listen to the lecture entitled: ‘Ischemia, Injury, Infarction’
2. Practice with interactive online exercise:
https://ekg.academy/learn-ekg?courseid=323&seq=1
3. Watch Bates OSCE video #1: Chest Pain, and then respond to the prompt below.
https://batesvisualguide.com/MultimediaPlayer.aspx?multimediaid=6017060
You have just watched a visit for a woman presenting with chest pain. In the space below, write a SOAP
note for this patient just as you would if you had been the nurse practitioner in this encounter. This
activity will help to reinforce the approach to a patient with chest pain so that you will feel more
confident when you encounter such a patient in your clinical placements.
BATES’ VISUAL GUIDE TO PHYSICAL EXAMINATION
OSCE 1: Chest Pain
This video format is designed to help you prepare for objective structured clinical examinations, or
OSCEs.
You are going to observe and participate in a clinical encounter of a patient who comes to the office
with a complaint of chest pain.
As you observe the encounter, you will be asked to answer questions while the image on the screen
freezes. Such questions will allow you to practice history taking and physical examination skills as well as
your clinical reasoning skills in developing an assessment or differential diagnosis and a plan—that is, an
appropriate next diagnostic workup.
You will have time to record your findings and receive feedback.
Health History
Tell me your special concerns today.
I’m a little worried because I have been having sharp pains in my chest for the last two weeks.
What findings might be important to look for as you observe this patient?
Level of distress.
Labored breathing.
Skin color: central and peripheral cyanosis.
Respiratory rate.
Two weeks ago I was reading a story in the paper about a car crash, when I noticed sharp pains in my
left chest. I was sweating and short of breath for about 5 minutes. And my heart felt like it was racing.
What possible causes of chest pain are you considering?
Angina.
GERD.
Panic attack.
Musculoskeletal chest wall pain.
Can you tell me how severe the pain was, on a scale from 1 to 10, with 1 being very faint and 10 being
severe?
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Page 1
I was 5 over 10.
Did it move into your neck or down your left arm?
No, no it was just in my chest.
How have you been since then?
I’ve had two other episodes, one of them was about 10 days ago when I was lifting some books, the
other was about 5 days ago when I was talking with my sister about our father’s death. He died 3
months ago in a car crash.
Did you have any other symptoms when you had these chest pains?
Yes, I had the same sweating and shortness of breath, with some light‐headedness during the most
recent one.
What was the level of pain?
The same, about 5 out of 10 for about 5 minutes. Then the pain just went away while I was sitting there.
I keep feeling so lost and panicked since my father died.
How are you feeling today?
Today I’m feeling fine, but I haven’t been sleeping well. It’s strange, I never felt anxious or depressed
before.
What cardiovascular risk factors do you need to consider in this patient? And which one has the highest
risk for coronary artery disease?
The risk factors are:
Family history of coronary artery disease.
Hyperlipidemia, hypertension, smoking, diabetes.
For women, preeclampsia and collagen vascular disease.
Family history conveys highest risk.
Do you have any problems with acid reflux? Or have you done any heavy lifting or strenuous exercise?
No, I’ve never had any stomach problems and I don’t really exercise much.
Do you have a history of high blood pressure? I noticed today your blood pressure was 140 over 95.
Yes, well I did have high blood pressure during my three pregnancies, I think it was about 145 over 90,
but the deliveries were fine.
What about smoking?
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When I was in my 20s I smoked about a pack a day for about 4 years.
Do you drink any alcohol?
I have 1…or 2 glasses of wine maybe 3 nights a week, more recently to help me relax.
Is there any heart disease in your family?
Yes, my brother had bypass surgery when he was 48, and my mom died of a heart attack when she was
62.
What about high cholesterol, or is there any diabetes in the family?
No, I’ve never had trouble with my cholesterol and we don’t have diabetes in my family.
You’ve given me a good picture of your symptoms, and I can see why you’re concerned. Is there
anything you think we may have missed?
No, but I can’t get away from these flashbacks about my father’s accident.
It’s common to visualize scenes like a crash with a loved one. Let’s do your physical examination, and
then we can talk more.
Physical Examination
I see your blood pressure is 150 over 95 and your heart rate is 95 today. These are both somewhat
elevated. I would like to begin by examining your lips and nails for color and then listen to your lungs.
Okay.
Examine lips and nails for cyanosis.
Okay, looks good.
Percuss then auscultate posterior lungs in ladder pattern.
Take a deep breath.
Listen to the lungs making sure to listen to the right middle lobe under axilla.
One more time.
[BREATHING IN AND OUT]
I’ll be examining the vessels in your neck, and then your heart. So please lie back with your feet straight
out.
Examine the neck first.
Assess the jugular venous pressure.
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Find the highest point of oscillation in the internal jugular vein…
…and measure the vertical distance from the sternal angle.
Palpate carotid upstroke.
The normal upstroke is brisk, smooth, and rapid, and follows S1 almost immediately.
Large bounding upstrokes indicate aortic insufficiency.
Listen for a bruit, which is a whooshing, murmur‐like sound often from atherosclerotic narrowing of the
carotid artery. A bruit sounds like this:
[BRUIT, WHOOSHING MURMUR]
Okay, I’m going to check the tapping impulse point of your heart.
Palpate the point of maximal impulse. You can do this and listen to the heart sounds by listening under
the gown without exposing the chest.
You may notice “tapping” which is timed at the beginning of systole. The point of maximal impulse may
be sustained or diffuse, meaning spread over more than one intercostal space.
Listen for S1 and S2 in each of the six listening areas: in the aortic area in the right second interspace
close to the sternum; in the pulmonic area in the left second interspace close to the sternum; in the left
third interspace; in the tricuspid area in the left fourth and left fifth interspaces; and in the mitral area at
the apex.
Use the diaphragm at the right upper sternal border and the lower left sternal border.
Use the bell at the apex.
Listen to and palpate the abdomen.
The following findings may be heard in the cardiac auscultation of this patient. Can you identify these
heart sounds?
[HEARTBEAT]
S4 is a low pitched diastolic sound reflecting changes in ventricular compliance, best heard with the bell
with the patient in a left lateral decubitus position. It may be present during ischemia or in the setting of
hypertension.
Identify these heart sounds.
[HEARTBEAT]
Mitral regurgitation is a holosystolic murmur reflecting mitral valve dilatation, best heard at the apex
that may radiate to the axilla and lower left sternal border. It may occur with transient ischemia.
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Assess congestive heart failure (CHF) in patients with extensive myocardial infarction that compromises
cardiac output due to decreased stroke volume or heart rate. Which findings on the cardiac exam have
the best evidence for congestive heart failure?
Rales, an elevated JVP, and an S3 consistently predict heart failure.
[HEARTBEAT]
S3 is a low‐pitched diastolic sound reflecting changed ventricular compliance, best heard with the bell
with the patient in a left lateral decubitus position.
Palpate the ankles for edema.
Diagnostic Considerations
List your diagnostic considerations in order of importance and explain your rationale.
Press pause and list your answers. Resume when you are ready to receive feedback.
Angina. This woman has stress‐induced non‐exertional chest pain. Recent evidence shows that women
present with more subtle symptoms of cardiovascular disease. She has cardiac risk factors of
hypertension, past smoking, preeclampsia, and family history.
Panic attack. She had stress related symptoms and flashbacks to the recent death of her father in a car
accident. She has suggestive anxiety, chest pain, and diaphoresis.
GERD. Her alcohol intake has recently increased. She has some reflux symptoms but her symptoms are
not triggered by meals and she does not report heartburn.
Musculoskeletal chest wall pain. There is no history of chest pain triggered by movement of the upper
torso or related exercise, and no notation of chest wall tenderness.
Dissecting aortic aneurysm. There is no asymmetry of blood pressures noted and no history of pain
shooting into the neck, up the side of the head, or into the back.
Diagnostic Workup
List 5 next steps in your diagnostic workup.
Press pause and list your answers. Resume when you are ready to receive feedback.
EKG. About 80% of patients with an acute MI have an initial EKG that shows evidence of new infraction
or ischemia, if read correctly. However, among patients mistakenly discharged from the emergency
department, up to 50% have normal or non‐diagnostic EKG findings.
Stress echo. This is the test of choice for women with atypical chest pain. The echocardiography stress
test has a sensitivity of 90% and specificity of 79% for women, and 85% and 96% for men.
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Page 5
Consider a trial of a proton pump inhibitor for 4‐6 weeks for possible GERD.
Chest x‐ray may be helpful to look for widened mediastinum, which can be evidence of aortic dissection.
Behavioral therapy—to learn management strategies for anxiety and panic disorder.
Summary
In sum, this is a 50‐year old school counselor with three episodes of left substernal chest pain over the
prior two weeks, rated 5 to 10 in intensity, with associated sweating and shortness of breath.
The first episode was precipitated by reading about a car crash, the cause of her father’s recent death.
The patient had hypertension during pregnancy and a brief smoking history in her 20s.
There is a strong family history of coronary artery disease. Her mother died of a myocardial infarction at
age 62 and her brother had a coronary bypass at age 48.
There is no history of diabetes. Her physical examination is unremarkable except for her blood pressure
of 150 over 95.
The differential diagnosis includes angina, especially suspect due to her symptoms, history of
hypertension during pregnancy, and family history. It also includes panic attack, GERD, musculoskeletal
chest pain, and dissecting aortic aneurysm.
The diagnostic workup includes an EKG, stress echo, trial of a PPI, chest x‐ray, and behavioral therapy.
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Page 6
Official reprint from UpToDate®
www.uptodate.com ©2020 UpToDate, Inc. and/or its affiliates. All Rights
Reserved.
Basic principles of electrocardiographic
interpretation
Author: Ary L Goldberger, MD
Section Editor: David M Mirvis, MD
Deputy Editor: Gordon M Saperia, MD
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Jan 2020. | This topic last updated: Jul 16, 2019.
INTRODUCTION
The electrocardiogram (ECG) is a graphical record of electric potentials
generated by the working heart muscle fibers during each cardiac cycle. These
low-amplitude potentials are detected on the surface of the body using
electrodes attached to the extremities and chest wall, and are then amplified
by the electrocardiograph machine and displayed on special graph paper
and/or on display monitors. A variety of systems are available for storage of
vast amounts of digital ECG data as part of electronic medical records.
This topic will review the basic aspects of ECG interpretation, including:

The cardiac electrical cycle

ECG waveforms and intervals

ECG leads

Genesis of the normal ECG
Each of these issues is discussed in greater detail in published reviews [1-3].
THE CARDIAC ELECTRICAL CYCLE
The initiating event for cardiac contraction is the spread of depolarizing
electrical currents through the heart. These currents are produced by three
types of cells: cardiac pacemaker cells, specialized conduction tissue, and the
heart muscle itself. The surface electrocardiogram (ECG), however, only
records the depolarization and repolarization potentials generated by the
“working” atrial and ventricular myocardial fibers.
The depolarization stimulus for the heartbeat normally begins in the sinoatrial
(SA) or sinus node, a collection of pacemaker cells with spontaneous
automaticity (figure 1) (see “Normal sinus rhythm and sinus arrhythmia”,
section on ‘Anatomy’). The initial phase of cardiac electrical activation consists
of the spread of the depolarization wave through the right and left atria,
resulting in atrial contraction. As the impulse reaches the base of the intraatrial
septum, it also stimulates pacemaker and specialized conduction tissues in the
atrioventricular (AV) nodal and His-bundle areas. Together, these two regions
constitute the AV junction.
The bundle of His splits into two main branches: the right and the left bundles.
The main left bundle bifurcates into two primary subdivisions: a left anterior
fascicle; and a left posterior fascicle. The bundle branches and fascicles
rapidly transmit depolarization wavefronts to the myocardium by way of
Purkinje fibers that penetrate the ventricular walls to excite the working
ventricular myocardial cells. The depolarization wavefronts spread through the
ventricular wall, from endocardium (inner layer) to epicardium (outer layer),
triggering intracellular calcium release and myofilament contraction
(electromechanical coupling).
ECG ELECTRODES AND LEADS
Electrodes are the sites at which an electrical potential is measured, while
electrocardiogram (ECG) leads record the difference in potentials between two
electrodes.
Electrodes — Standard surface electrodes (right and left arm, right and left
leg, and the six precordial electrodes) measure the electrical potential at a site.
In addition, a reference site, the central terminal of Wilson, is calculated from
the average voltage of the limb leads. This idealized site is meant to represent
a reference at the center of Einthoven’s triangle where total current is zero.
The central terminal is referred to as the reference or indifferent electrode.
Unipolar ECG leads are derived from the difference between the measured
voltage at a surface electrode and the calculated voltage at this central
reference point.
ECG leads — The 12 conventional ECG leads record differences in electrical
potentials, either between two surface electrodes (bipolar leads), or between a
surface electrode and the central terminal of Wilson (unipolar leads).
ECG leads are divided into two groups: six extremity (limb) leads and six chest
(precordial) leads. The extremity leads record potentials transmitted onto the
frontal plane and the chest leads record potentials transmitted onto the
horizontal plane (figure 2).
Limb leads — The six extremity, or limb, leads are further subdivided into
three “bipolar” leads (I, II and III) and three “unipolar” leads (aVR, aVL and
aVF). Each bipolar lead measures the difference in potential between
electrodes at two extremities, with one electrode connected to the positive pole
and the other to the negative pole of the voltmeter:

Lead I records the difference between potential sensed by the electrode
placed on the left arm (the positive pole) and one placed on the right arm
(negative pole).

Lead II records the difference between electrodes on the left leg (positive)
and the right arm (negative).

Lead III records the difference between electrodes on the left leg (positive)
and the left arm (negative).
These were the leads of the original string galvanometer, the forerunner of the
modern electrocardiograph introduced by the Dutch physiologist, Dr. Willem
Einthoven at the beginning of the 20th century.
The “unipolar” limb leads, in comparison, measure the cardiac voltage (V) at
one site relative to the central terminal, which has approximately zero
potential. Thus:

Lead aVR records right arm potentials

Lead aVL records left arm potentials

Lead aVF records left leg (foot) potentials.
The lower case “a” indicates that these potentials are augmented by 50
percent. The right leg electrode functions as a ground.
The spatial orientation and polarity of the six frontal plane leads is represented
on the hexaxial diagram (figure 3). As examples, lead I is primarily a left-right
lead, while aVF is an inferior-superior lead.
Precordial leads — The six standard chest, or precordial, leads are also
unipolar recordings. They represent the voltage difference between the central
terminal and electrodes placed in the following positions (figure 4):

V1 – 4th intercostal space (ICS), just to the right of the sternum

V2 – 4th ICS, just to the left of the sternum

V3 – midway between V2 and V4

V4 – 5th ICS in the mid-clavicular line

V5 – anterior axillary line, same level as V4

V6 – mid-axillary line, same level as V4 and V5
Inadvertent misplacement of chest leads is quite common and can lead to
considerable diagnostic confusion.
The ECG leads are designed so that a positive (upright) deflection will be
recorded in a lead if a wave of depolarization spreads toward the positive pole
of that lead. A negative deflection will be recorded if the wave of depolarization
spreads toward the negative pole of any lead (ie, away from the positive role).
As an example, depolarization spreading to the left and posterior will produce
a positive deflection in lead I (a left-right lead) and a negative deflection in lead
V1 (an anterior-posterior lead). If, however, the mean orientation of the
depolarization vector (or electrical axis) is at right angles to a given lead axis, a
small biphasic (equally positive and negative) deflection will be recorded.
Together, the frontal and horizontal plane electrodes provide a threedimensional report of cardiac electrical activity. Each lead can be likened to a
different video camera angle “looking” at the same dynamic events — atrial
and ventricular depolarization and repolarization — from different spatial
orientations. The standard 12 lead ECG can be supplemented with additional
leads under special circumstances. In special circumstances, additional
precordial leads may provide information. For example, right chest leads V1R
to V6R (where V1R corresponds to V2 and V2R to V1, etc) are routinely
obtained in cases of suspected acute right ventricular infarction, associated
with inferior ST elevation myocardial infarction. Leads V7 to V9 may be useful
in detection of postero-lateral ST elevation myocardial infarction. (See “Right
ventricular myocardial infarction”.)
ECG WAVEFORMS AND INTERVALS
Electrocardiogram (ECG) waves are labeled alphabetically starting with the P
wave, which represents atrial depolarization (figure 5). The QRS complex
represents ventricular depolarization and the ST-T-U complex (ST segment, T
wave and U wave) represents ventricular repolarization. The J point is the
junction between the end of the QRS and beginning of the ST segment. (Atrial
repolarization occurs during the PR segment and QRS complex but is usually
of too low an amplitude to be detected, but may become apparent in
conditions such as acute pericarditis or atrial infarction.)
The QRS-T waveforms on the surface ECG correspond in a general way to
the different phases of simultaneously obtained ventricular action potentials,
the intracellular recordings from single myocardial fibers (figure 6). (See
“Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic
drugs”.):

QRS onset corresponds to the rapid upstroke (phase 0) of the action
potential.

The isoelectric ST segment corresponds to phase 2 of the action potential
(plateau phase), during which myocardial fibers normally achieve about
the same potential.

The T wave corresponds to phase 3 of the action potential (active
repolarization).

The isoelectric segment between the end of the T wave and the next
depolarization corresponds to phase 4 of the action potential (recovery).
Factors that decrease the slope of phase 0 by, for example, impairing the
influx of sodium tend to increase QRS duration (eg, severe hyperkalemia or
drugs such as quinidine, flecainide, or propafenone). On the other hand,
factors that prolong phases 2/3 (eg, hypocalcemia or drugs such as
amiodarone, dofetilide, or sotalol) increase the QT(U) interval. In contrast,
factors such as digitalis and hypercalcemia shorten ventricular repolarization
(phase 2) and abbreviate the ST segment.
The ECG waves are recorded on special graph paper which is divided into 1
mm2 grid-like boxes. The ECG paper speed is ordinarily 25 mm/sec. As a
result, each 1 mm horizontal box corresponds to 0.04 second (40 ms), with
heavier lines at larger 0.20 sec (200 ms) intervals. Vertically, the ECG graph
measures the height (amplitude) of a given wave or deflection, as 10 mm
equals 1 mV with standard calibration.
ECG intervals — There are four major sets of ECG intervals: R-R (inversely
related to the pulse or heart rate), PR, QRS, and QT/QTc (figure 5). The
instantaneous heart rate (beats/min) can be readily computed from the
interbeat (R-R) interval by dividing the number of large (0.20 sec) time units
between consecutive R waves into 300 or, for more precise measurement, the
number of small (0.04 sec) units into 1500.
Note that the P-P interval in sinus rhythm with 1:1 atrioventricular (AV)
conduction (“normal sinus rhythm”) can also be measured and will be equal to
the R-R interval. However, in certain circumstances, notably sinus rhythm with
second or third degree AV block, the P-P and R-R intervals will not be the
same. In the two arrhythmias characterized by continuous atrial activity,
namely atrial flutter and atrial fibrillation, there are no true P-P intervals; but the
atrial cycle lengths will be much shorter than the R-R intervals in such cases
due to atrial depolarization rates ≥250/min. (See “ECG tutorial: Atrioventricular
block” and “Electrocardiographic and electrophysiologic features of atrial
flutter”.)
The PR interval measures the time (normally 0.12 to 0.20 sec; 3 to 5 small
boxes) between the onset of atrial and ventricular depolarization. This includes
the physiologic delay imposed by stimulation of cells in the AV junction area.
The QRS interval (normally ≤0.10 sec = 2.5 small boxes measured by hand, or

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