Education Committee Newsletter
Down and Dirty EKGMichelle Earl
Essentials of Cardiovascular Nursing at
The Medical Center of the Rockies
presented by Lisa Soltis, MSN &
educator for MED-ED, explained an easy
method for visualizing where 12 Lead
EKG changes are occurring in the heart.
1st Consider how the heart lays in the
chest: slightly anteriorly rotated &
laying on its right side.
2nd Think of leads, AVL,AVF,I,II,III as
views from a camera lens looking into
the heart as they sit on the face of a
clock.
AVL: Looks in & down from the L
shoulder @ 1:00
I: Looks in laterally @ 3:00
II: Looks inferiorly towards the heart @
5:00
AVF: Looks up inferiorly from the feet @
6:00
III :Looks from the Right to the inferior
aspect @7:00
3rd The V leads are the views directly
over the heart as the sit on the chest
during the EKG.
V1: Right Septal area
V2:Left Septal area
V2,V3,V4: Looks at the Anterior Left
Ventricular area
V5,V6: Looks at the Left lateral aspect.
Hopefully ,visual learners will find this
approach to 12 Lead EKG interpretation
easier to “see”.
Torsades: Becky Davis
Torsades De Pointes (TdP) - is a form of
Polymorphic VT which can occurred due
to congenital long QT syndrome or be
acquired. The definition of torsades is a
EKG TOPICS
ventricular rhythm which is faster than
100 beats per minute and has frequent
variations of the QRS axis. Most TdP,
has a progressive cyclical rotation or
twist around the line hence the name
Torsades De Point – “twisting around
the points”.
The usual presentation of TdP is a
preceding prolonged QT interval in the
last sinus beat which precedes the
arrhythmia, shown with a ventricular
rate between 160 – 250 beats per
minute, with irregular RR intervals, and
cycling of the QRS Axis through 180
degrees every 5 t0 20 beats. Usually the
rhythm is short lived but can happen
multiple times in a patient. The patients
with this rhythm can potentially have
the rhythm deteriorate to ventricular
fibrillation and sudden cardiac death.
Other risk factors that could cause TdP,
hypokalemia, hypomagnesemia, and
hypocalcemia. These can be seen in
those patients taking antiarrhythmics,
nutritionally malnourished individuals
for example alcoholics and anorexic
patients.
Treatment for Torsades De
Points depends on the presentation of
the TdP. Frequently if it is drug induced
patients develop prolonged QT, will be
watched on an outpatient basis and
changes in medication to decrease the
prolonged QT. Frequently these
patients will have Holter monitor or
frequent intermittent EKGs to follow up.
Any evidence of EKG instability,
ventricular ectopy, widening QRS, TdP
will require the patient to be admitted
and telemetry observation for
problems.
Acute treatment of the patient who is
awake and alert with TdP, is a brief trial
of medical therapy. IV magnesium
Sulfate is first line therapy for all TdP.
Standard regimen is 2 grams 50%
magnesium sulfate IV bolus over 2
minutes. If continues follow in 15
minutes with another bolus.
Temporary transvenous overdrive
pacing (atrial or ventricular) can be
used for those patients who do not
respond.
Isoproterenol can be used according
AHA guidelines for persistent TdP.
For the thermodynamically unstable
patient or unconscious patient,
immediate defibrillation is required.
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Finally, Brady Arrhythmias can also
cause TdP and frequently these patients
will have to be paced.
Afib/Flutter-Amanda Puhal
Flutter
A-fib
Afib and aflutter are atrial arrhythmias.
Afib is a fast and irregular(unorganized)
heart rate/rhythm. Aflutter differs from
afib by being fast and regular. Common
causes are alcohol use, CAD, hx of MI or
bypass surgery, heart failure, valve
disease, htn, medications, thyroid
problems, pericarditis, or sick sinus
syndrome. Afib can start or stop
suddenly on its own. Sometimes
cardioversion is required to get the
heart back into a normal rhythm or
medications. In chronic afib it is
important the patient is on blood
thinners to decrease the risk of stroke.
STEMI/NSTEMI-Erin Pillette
STEMI
-Infarction with troponin elevation.
-Developing complete occlusion of
major coronary artery with full thickness
damage to the myocardium.
-Approx 70% of AMI population
Diagnosis:
EKG => ST Depression, transient ST
elevation, T-wave inversion
CK-MB => Rises after 4-6hrs and falls to
normal after approx. 48-72hrs
Troponin => Rises after 4-6hrs and
remains elevated for up to 2wks
Chest Xray => Assess for lung edema
Echo => Assess for ventricular function
and other complications
Treatment:
-Bed rest with continuous EKG
monitoring
-Oxygen therapy
-Analgesia for pain control – i.e.
morphine
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-Antiplatelet therapy such as Aspirin
- ASA reduces mortality by 25%
-Anticoagulation therapy such as
heparin or fragmin
-Beta Blockers– to reduce arrhythmias,
heart rate, bp, myocardial oxygen
demand, and relieve pain
-Nitrates– to vasodilate and relieve pain
-Statins– no matter if cholesterol levels
are elevated or not
-ACE Inhibitors or ARBs
- ACE Inhibitors help prevent heart
failure, reduce recurring infarctions, and
reduce ventricular remodeling
- ARBs can be used as alternatives to
ACE Inhibitors
-Reperfusion Therapy => within 120min
Fibrinolytics ARE beneficial
NSTEMI
-Ischemia with troponin elevation.
-Developing complete occlusion of
minor coronary artery or partial
occlusion of major coronary artery
causing partial thickness damage to
myocardium
-Approx 30% of AMI population
Diagnosis:
EKG => ST Elevation, pathological Qwave, T-wave inversion
CK-MB => Rises after 4-6hrs and falls to
normal after approx. 48-72hrs
Troponin => Rises at 4-6hrs and remains
high for up to 2wks
Chest Xray => Assess for lung edema
Echo => Assess for ventricular function
and for other complications
Treatment:
-Bed rest with continuous EKG
monitoring
-Oxygen therapy
-Analgesia for pain control – i.e.
morphine
-Antiplatelet therarpy such as Aspirin
-Anticoagulation therapy such as
heparin
-Beta Blockers – to reduce arrhythmias,
heart rate, bp, myocardial oxygen
demand, and relieve pain
-Nitrates – to vasodilate and relieve pain
-Statins – no matter if cholesterol levels
are elevated or not
-ACE Inhibitors or ARBs
- ACE Inhibitors help prevent heart
failure, reduce recurring infarctions, and
reduce ventricular remodeling
- ARBs can be used as alternatives to
ACE Inhibitors
-Angiography for further diagnosis
Fibrinolytics ARE NOT beneficial
EKG TOPICS
RBBB/LBBB-Tre Andres
In RBBB, the right bundle branch no
longer conducts electricity normally,
and the heart's electrical impulse enters
the ventricles using only (or mainly) the
left bundle branch - which means the
left ventricle receives the electrical
impulse first. Then, from the left
ventricle, the electrical impulse finally
makes its way to the right ventricle. As a
result, the two ventricles no longer
receive the electrical impulse
simultaneously. First the left ventricle
receives the electrical impulse, then the
right. RBBB is a relatively common ECG
finding, and while it occurs in a variety
of medical conditions, it also is found in
some people whose hearts are
completely normal - in which case RBBB
usually has no medical significance.
While the presence of RBBB means that
the right ventricle begins to contract
slightly after the left ventricle, in normal
hearts this delay in right ventricular
contraction causes no measurable
decrease in cardiac function. So in
general isolated RBBB has no apparent
medical significance, and usually can be
written off as a "normal variant" and
safely ignored. However, we should
always educate patients to follow up
with their PCP for a repeat EKG in 4-6
months.
With a LBBB the left bundle branch no
longer conducts electricity normally. So
the electrical impulse enters the
ventricles through the right bundle
branch, and is carried first to the right
ventricle (first panel). From there, it
finally spreads to the left ventricle
(second panel). Once again, the two
ventricles no longer receive the
electrical impulse simultaneously. First
the right ventricle receives the electrical
impulse, then the left. LBBB is
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somewhat less common than RBBB, and
its presence usually indicates underlying
cardiac pathology. LBBB is commonly
seen with dilated cardiomyopathy,
hypertrophic cardiomyopathy,
hypertension, aortic valve disease, CAD,
and a variety of other cardiac
conditions. While occasionally LBBB
occurs in apparently healthy people, its
appearance should trigger a thorough
search (as opposed to a simple
screening) for underlying cardiac
problems, a new LBBB could be
indicative of an MI. If the cardiac
evaluation reveals no underlying heart
problems, the medical significance of
LBBB (especially in young people) is
generally regarded as minimal.
PEA-Jen Comer
Pulseless electrical activity, PEA, is any
organized rhythm without a pulse. This
is not a shockable rhythm and requires
immediate high quality CPR and
intiation of ACLS guidelines for PEA.
After gaining IV access, vasopressors,
including Epinephrine and one dose of
Vasopressin, are given simultaneously
with CPR. If the PEA rate is slow,
consideration may be given for dosing
with atropine. Other medications may
be given depending on the suspected
cause of the PEA arrest. These patients
have poor outcomes and their best
chance of survival is to identify any
reversible problems that may be causing
the PEA. Consider frequent causes of
PEA by recalling the H’s and T’s
presented below. Analyzing the ECG
may provide clues to the underlying
cause of the PEA. Gathering information
from friends/family could help
recognize a drug overdose/poisoning.
This patient population outcome
depends solely on the ability of the
team to provide effective CPR and
identify and correct the cause of the
PEA arrest. During resuscitation, the
patient may go into VF or pulseless VT.
This is a shockable rhythm and requires
following the VF/VT pathway on the PEA
algorithm.
Education Committee Newsletter
H’s
T’s
Hypovolemia
Toxins
Hypoxia
Hydrogen
(acidosis)
Hyperhypokalemia
Hypoglycemia
ion
Tamponade
(cardiac)
Tension
pneumothorax
Thrombosis
(corona
ry and
pulmon
ary)
Trauma
Hypothermia
Narrow Complex/Rapid Rate could
indicate hypovolemia, cardiac
tamponade, tension pneumo-thorax,
or lung thrombosis.
Slow Rate would indicate hypoxia which
could be related to a tension pneumo.
Prolongation of QT interval would be
indicative of drug overdoses or
hypokalemia.
WPW-Daryl Johnson
Wolff-Parkinson-White syndrome is a
heart condition in which there is an
abnormal extra electrical pathway of
the heart. The condition can lead to
episodes of rapid heart rate
(tachycardia).
Wolff-Parkinson-White syndrome is one
of the most common causes of fast
heart rate disorders in infants and
children.
In people with Wolff-ParkinsonWhite syndrome, some of the heart's
electrical signal goes down an extra
(accessory) pathway. This may cause a
very rapid heart rate called
supraventricular tachycardia.
Most people with Wolff-ParkinsonWhite syndrome do not have any other
heart problems. However, this condition
has been linked with other conditions,
such as Ebstein's anomaly. There is also
a form that runs in families.
Symptoms
How often the rapid heart rate occurs
depends on the patient. Some people
with Wolff-Parkinson-White syndrome
may have just a few episodes of rapid
heart rate. Others may have the rapid
heart rate once or twice a week or
more. Sometimes there are no
symptoms, and the condition is found
when a heart test is done for another
EKG TOPICS
reason.
Spring 2014
Invitation to February’s CARDIAC
CONSULT:
A person with this syndrome may have:
Chest pain or chest tightness
Dizziness
Light-headedness
Fainting
Palpitations (a sensation of feeling your
heart beat)
Shortness of breath
Signs and tests
Wolff-Parkinson-White syndrome may
be diagnosed through continuous
ambulatory ECG monitoring, such as
with a Holter monitor.
A test called an electrophysiologic study
(EPS) is done using catheters that are
threaded up to the heart from an IV
placed in the leg. It may help identify
the location of the extra electrical
pathway.
Treatment
Medicine such as adenosine,
antiarrhythmic drugs, and amiodarone
may be used to control or prevent a
rapid heartbeat.
If the heart rate does not return to
normal with medication, doctors may
use a type of therapy called electrical
cardioversion (shock).
The long-term treatment for WolffParkinson-White syndrome is catheter
ablation. This procedure involves
inserting a tube (catheter) into an artery
through a small cut near the groin up to
the heart area. When the tip reaches
the heart, the small area that is causing
the fast heart rate is destroyed using a
special type of energy called
radiofrequency.
Open heart surgery to burn or freeze
the extra pathway may also provide a
permanent cure for Wolff-ParkinsonWhite syndrome. However, surgery is
usually done only if you need surgery
for other reasons.
Expectations (prognosis)
Catheter ablation cures this disorder in
most patients. The success rate for the
procedure ranges between 85 and 95%.
Success rates will vary depending on the
location and number of extra pathways.
SVT-Kellie Callahan
What: When the Heart beats
abnormally (at least 100 BPM, up to 300
BPM). A sudden start to the fast rhythm,
and an abrupt stop, classify SVT. There
are times in which patients dealing with
SVT will have palpitation, syncope,
bounding pulse, chest pain, nausea, and
sweating. When patients become
symptomatic, decreased mental status,
decreased palpable pulse, immediate
intervention is necessary.
When: Faulty electrical connections
made in the heart misfire. (Always at or
above the Bundle of His) hence, the
name SUPRA VENTRICULAR) Many
different factors can cause SVT,
including ephedrine; ETOH, caffeine or
other stimulants. Other causes of SVT
can include respiratory complications,
such as pneumonia, and COPD.
Where: Patients can go into SVT any
time, and anywhere. It is appropriate as
nurses, that we teach patients signs and
symptoms of this hear irregularity,
especially if the patient has been seen
by a doctor for this in the past. Patients
will often times be asked by their
primary doctor to wear an “event
monitor.” The patient will wear such
device for a prescribed amount of time,
when in which if the patient feels any
palpitations, chest pain, nausea,
vomiting, near syncope or rapid heart
rate, the patient will push a button on
the monitor, which alerts the patient’s
MD electronically. At this point, they
can read the patient’s EKG for that
period of time, and determine if any
irregularities exist.
HOW TO TREAT!
The most common and non-invasive
attempted treatments of SVT include…
Vagal Maneuvers (stimulating the
Vagus nerve promotes slowed
conduction of electrical impulses, which
will slow the heart rate.) Vagal
maneuvers include:
-Bearing down
-Blowing through a straw
-Coughing
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Adenosine (this medication is a part of
the ACLS algorithm for SVT) before you
give adenosine you must…..
Place patient on Zoll (cardiac pads)
Have 2 Large bore AC IV’s established
IV Saline hanging and infusing with NS
flushes to be given immediately after
drug admin
Continuous EKG to determine if patient
is in SVT (adenosine is given to slow the
rate, so one can look at the underlying
rhythm)
Cycle blood pressure frequently Q3
minutes, have patient on nasal cannula
2L of O2 for comfort
EXPLAIN TO PATIENT THEY WILL FEEL
FUNNY FOR A SHORT AMOUNT OF
TIME, BUT THOSE FEELINGS WILL PASS.
Attending and Resident at bedside, wait
for MD to give verbal start of
medication administration.
DOSE: 6mg Adenosine if that doesn’t
work, repeat with 12mg of Adenosine. If
patient remains in SVT, repeat once
more with 12mg of Adenosine. If still in
SVT and patient becomes further
symptomatic, then move to
Cardioversion.
Cardioversion This is typically the last
effort to break the patient’s arrhythmia
of SVT. At this point, the patient has
started to decompensate, ie: unsafe
decrease in BP, decrease mental status,
general condition of the patient. The
MD will decide if cardioversion is
necessary. At this point, you should
have tried vagal maneuvers and
Adenosine without any relief in
symptoms. The patient will already be
on the Zoll pads, BP cycling, continuous
EKG, 2 large bore AC IV’s, 2L O2 via NC,
and the primary RN will be educating
patient regarding expectations. If time
allows, the patient usually receives
some pain medication, or sedative to
ease the pain of the shock they are
about to receive.
EKG TOPICS
Sinus Tachycardia-Ryan
Morissette
Sinus tachycardia is a
commonly seen heart rhythm in the
emergency department and can be
caused by multiple factors. Usually this
is a benign (asymptomatic) rhythm
defined as a heart rate greater than 100
beats per minute (rarely greater than
160bpm), but can depend on age and
physical status of patient. If the rate
increases, less time is allowed for
ventricular filling, and cardiac output
and blood pressure can potentially be
reduced. ST usually presents with
increased blood pressure and cardiac
output as a hyperdynamic rhythm but
can decrease with decompensation.
Most ST in ER patients is commonly
caused by pain, fever, anxiety,
dehydration, infection, drugs,
withdrawal, hypoxia, anemia, exercise
and many other factors.
We usually see ST as a
compensatory mechanism to increase
cardiac output. This is caused by
catecholamine release, such as
epinephrine, norepinephrine, and
dopamine, which act to increase
impulses from the sinoatrial node to
increase the ventricles rate and
contractility. The rhythm itself will
appear regular, rate greater than
100bpm, have normal P wave, PR
interval, QRS complex, and T wave and
configuration should be normal but may
have a shortened QT. As the rate
increases, the structures can become
superimposed on each other and be
difficult to identify and interpret.
Generally, treatment is not
needed but can include interventions
for correcting reasons the patient is
experiencing tachycardia. Interventions
can include treatment for pain, anxiety,
IV fluids for dehydration, antibiotics for
infections, antipyretics, sedatives,
correcting electrolyte imbalances,
administering oxygen or a combination
of therapies. The cause is usually
multifactorial and takes investigation to
figure out source with history and
physical, diagnostics, and blood work
and then to decide treatment options.
The important thing to
remember is that tachycardia (defined
by patient age and status) is not normal
for any average person and thus must
be investigated. The longer the patient
sustains this rhythm, the more their
reserves are depleted and their chance
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for a negative outcome can increase. It
really depends at which point on the
continuum they present to the ER and
the speed at which they are diagnosed
and treated. Quickly treating sinus
tachycardia can help to prevent
potentially life threatening
consequences where the tachycardia is
only a sign of a much deadlier
pathology.
Vfib-Nicholaus Mohr
Ventricular Fibrillation (V-Fib) is a heart
rhythm where the heart beats with
rapid erratic electrical impulses. This
causes your heart chambers to quiver
uselessly instead of contracting in an
organized fashion to pump blood to the
body. This in turn cuts off blood supply
to vital organs. Ventricular Fibrillation is
frequently triggered by a heart attack.
Symptoms include chest pain, rapid
heartbeat, dizziness, nasuea, and
shortrness of breath. Several factors
put you at risk such as a previous
episode of Ventricular Fibrillation, heart
attack history, heart muscle damage or
disease, and the use of illegal drugs such
as methamphetamines and cocaine.
Emergency treatments focus on
restoring blood flow to the vital organs
of the body, especially your brain. To
accomplish this, early defibrillation and
CPR are key. This will help get the heart
back into a normal rhythm and help
restore adequate cardiac output. Beta
Blockers are often used for long term
treatment of Ventricular Fibrillation.
Other possible drugs such as Ace
Inhibitors, Calcium Channel Blockers,
and Amiodorone are also used.
Implantable Cardioverter-Defibrillator
(ICD) can be implanted to help your
heart maintain a normal rhythm by
sending electrical impulses through your
heart to speed it up or slow it down.
Sinus Bradycardia-Dan Evans
Causes: SA node failure, athletic
conditioning, SSS, MI, endocarditis,
myocarditis, hypothyroidism,
hyperkalemia, hypertension, medication
overdose, beta blockers, antiarrhythmic
Symptoms: dizziness, SOB,
chest pain, hypotension,
confusion, AMS
Education Committee Newsletter
-
-
A heart block is a disease in the
electrical system of the heart. It can
cause lightheadedness, syncope and
palpitations.
First degree AV block

Spring 2014
Treatment: fluid challenge,
medications, external pacing,
correcting electrolyte
imbalances
Medications : Atropine, NS,
epinephrine
Heart Blocks-Catherine
Bergstrom


EKG TOPICS
Regular rate and rhythm
Lengthened PR interval (
>0.20 seconds)
No treatment
Third Degree AV block




Regular , but atrial and
ventricular rhythms are
independent
Atrial rate is usually faster
The atria and ventricles beat
independently
Need to implant pacemaker
Second degree AV block Type 1 (Mobitz
I or Wenchebach)



Irregular rhythm but with
progressively longer PR
interval
PR interval get progressively
longer until a QRS cycle
drops off
Cards consult
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Second Degree AV block Type 2
(Mobitz II)

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
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Atrial rate is regular (and
faster than ventricular rate),
ventricular rate is irregular
More P waves than QRSs
PR interval may be normal or
prolonged
QRS is normal or wide
Cards consult
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