Rebecca Sopelak

Simulation
Student Learning
Objectives:

Simulation
Expectations:

1. Identified primary nursing diagnosis

2. Implements patient safety measures
3. Evaluates patient assessment information including vital signs
4. Implements therapeutic communication
5. Implements direct communication with multidisciplinary team members
6. Demonstrates effective team work
7. Prioritizes and implements physician orders appropriately
8. Implement the 6 rights of medication administration
9. Implements a focused respiratory and/or cardiac assessment
10. Recalls indications and contraindications of oxygen therapy
11. Initiates relevant cardiac and respiratory monitoring and assessment
12. Demonstrates use of telemetry monitor as needed to recognize rhythm
13. Demonstrates and responds to scenarios which cause respiratory or cardiac arrest.
14. Initiates rapid response team for unstable patients and/or recognizes potentially unf
patient outcomes.
15. Initiates code blue response and provides appropriate interventions until the code t
arrives

Student roles and responsibilities

o Prepare for simulation through assigned readings:
Sole pages 221-245
o Read, sign & bring video and confidentiality agreement to assigned simulation
Time: available in CANVAS under Simulation Page.
Instructor expectations for the learners
o Treat the simulator as a real person (e.g. respect, sympathy, etc)
o Perform and verbalize skills
o Act in a professional manner at all times.
What to expect:
o The simulation closely mimics real-life. However, some things may appear so
artificial-as an example the ability to detect perfusion is unable to be m
in the
Manikin. Therefore, the purpose should be to focus on why the patien
decreased
Perfusion.
o You will not have a facilitator in the room during the simulation.
o There will be at least 3-4 students that work together as a team.
o Your performance will be video-taped-the video file may be used as part of th
Process.

Following simulation a debriefing will occur: the purpose of the debriefing is to discu
what went well and opportunities for improvement (review peer and individual respon

Rebecca Sopelak

Student
Orientation to
Simulator:

Assessment
o Ask all questions directly to the patient
o Vital signs & physical exam will be obtained from the patient
o Review BP auscultation, pulse sites, heart, lung, and bowel sounds
Interventions
o Airway: Oxygen, Bag-Valve Mask capability, ETT tube capability (7.5
size only)
o IV Access: Perform venipuncture in the Right ARM only (manikin-use
22 gauge only, verbalize what size you want)
Medication Administration:
o DO NOT administer intratracheal, intranasal, or intraosseous medicatio
Sim Man 3G.

Medication Cart
o Use the cart and scanner to administer medications. (has sign-in passwords on
the cart)

Rebecca Sopelak

Case Study
Write up responses
and bring on
simulation day to
turn into your
clinical instructor
Rebecca Sopelak

Mr. S., a 43-year-old male, was found unresponsive on the floor by two co-workers at the mec
shop where he was employed. He had been conversing with a co-worker 10 minutes earlier an
no apparent distress. One co-worker started cardiopulmonary resuscitation (CPR) and the oth
help. An automated external defibrillator (AED) was brought to the scene within 2 minutes. The
adhesive electrode pads were applied appropriately, and after rhythm analysis, one shock was
and delivered by the AED. CPR was resumed for 5 cycles/2 minutes. After 2 minutes, rhythm a
was performed by the AED and another shock was advised and delivered. The paramedics arr
assessed Mr. S. He was unresponsive with shallow respirations, heart rate 100 beats/minute in
sinus rhythm, blood pressure 90/52 mm Hg with a palpable carotid pulse. He was intubated fo
protection with 100% oxygen delivered through a bag-mask device. An intravenous (IV) line wa
the left antecubital vein, and 0.9% normal saline infusion was started.

On Mr. S.s arrival to the nearest emergency department, seizure activity was noted. The decis
made that Mr. S. met criteria for therapeutic hypothermia, and arrangements were made to tra
the medical center nearby.

On Mr. S.s arrival to the critical unit at the medical center, his rhythm converted from normal s
with a pulse, to pulseless electrical activity (PEA). CPR was initiated for 5 cycles/2 minutes an
rhythm remained PEA. CPR resumed and epinephrine 1 mg IV was given. After 5 cycles/2 min
CPR, a femoral pulse was palpated with normal sinus rhythm.
Describe in depth each question and provide how the nurse would be involved:

1. What is the correct method for using an AED after it is brought to an unresponsiv
patient(describe the process of applying and implementing the use of the AED)?

The first thing you would do when the AED arrives at the patient is put on the electrod
The pads can go on in two ways. One way is with both pads on the front of the ches
one of the pads goes on the upper right side of the chest, second intercostal space, j
the sternum and the other pad goes on the left, lower, lateral side of the chest, fifth in
space, near the apex of the heart. The second way for the pads to go on would be o
the left anterior precordial area and the other pad is placed at the left posterior-infras
area (Sole, 231). The pads are to never go over the patients nipple, a pacemaker, o
the patient is a female, you need to move her breast to place the pads on the left por
chest. You dont ever place the electrode on the breast. The next thing you would ne
to check and analyze for a rhythm. If there is not rhythm or electrical activity going th
heart, there is nothing to shock, so the only thing you can do for the patient is continu
try to treat the cause of the rhythm. If there is electrical activity, you need to determin
rhythm. Not all rhythms get defibrillated. When using an AED, the AED will analyze
for you once you place the electrode pads on the patient in their proper placements.
using a defibrillator on the crash cart, you will need to analyze the rhythm before proc
with a shock. The two rhythms that you defibrillate are Ventricular Fibrillation and Pu
Ventricular Tachycardia. Both of these are chaotic rhythms that show signs of electri
in the heart, but arent organized enough for you to be able to synchronize a shock to
rhythm. For these two you defibrillate as soon as possible. An AED will prompt you
the patient using a shock advisory notice, which then advises you to shock the patien
pressing a button. For a defibrillator on the crash cart, you would need to set the cha

Rebecca Sopelak

200J if it is biphasic, and 360J if it is monophasic). Before shocking the patient you n
clear the patient, make sure no one is touching him or her or the bed. The person do
needs to stop CPR and get away from the patient. Once the patient and bed are clea
administer the shock to the patient. If you dont not receive a response after you def
(and the patient is still in VF or pulseless VT), resume CPR for 2 more minutes, reche
rhythm, and shock again if necessary.

2. What are the inclusion criteria for therapeutic hypothermia (include an indepth di
each inclusion criteria)?

Therapeutic hypothermia is used for patients who have a cardiac arrest with a rhythm
ventricular fibrillation or asystole. In both cases, the patients cardiac rhythms preven
blood flow from moving throughout the body. In asystole, there is no blood flow in the
ventricular fibrillation the ventricles are quivering making it hard for the heart to effect
the blood out of the ventricles to the body. This results in brain injury and ischemia o
vessels from vasoconstriction. The brain injury and ischemia can result in fever. The
thats a result of brain damage can result in poorer neurological recovery due to the n
higher oxygen demand. Because of this, evidence based practice guidelines have id
therapeutic hypothermia as a way to prevent fever from occurring (Sole, 244). The p
therapeutic hypothermia is to decrease the body temperature to amount 32-34 degre
for a period of 12-24 hours. This allows a decrease in the bodys metabolic rate thus
the demand for oxygen and allowing the body to have time to improve the oxygen su
brain. With the improved oxygenation that was previously lost during the arrest, the b
recover neurologically. This allows for better outcomes and a higher chance to resto
patient to their level of functioning prior to the cardiac arrest.

3. What are potential causes of PEA (Describe in-depth discussion of all 10 causes

The potential causes of a PEA are hypovolemia, hypoxia, hypokalem

hyperkalemia, hypothermia, tension pneumothorax, cardiac tampon
toxins (drug overdoses), and thrombosis (pulmonary or coronary).

Hypovolemia: Hypovolemia is when there is a very low blood volum

body. When there is a low amount of blood in the body, there is not
sufficient amount of blood being returned to the heart. If the heart
have enough blood to pump out of the ventricles (decreased cardia
baroreceptors will trigger a response of vasoconstriction to try to ca
heart to increase systemic vascular resistance. ADH will also be rel
response to the low blood volume, triggered by the renin-aldosteron
angiotensinogen-system (RAAS), causing retention of sodium and fl
to increase the blood volume. These will temporarily help to increa
rate, contractility, and blood volume, thus helping increase cardiac
With this increase in the blood flow by the RAAS system and barore
responses, the heart requires more oxygen to keep up with the dem
Eventually the oxygen requirements become too much to meet the

Rebecca Sopelak

demands, the cardiac output and ejection fracture drops and the blo
pressure begins to fall again. The hypovolemia continues causing a
decrease in tissue perfusion, which can lead to ischemia and impair
cellular metabolism. This impaired cellular metabolism is what cau
problems in the cardiac muscle that leads to cardiac dysfunction an
dysrhythmias (Sole, 273). PEA is due to the impaired cellular metab
preventing the cardiac muscle from being able to contract and pum
heart. The electrical activity to stimulate the heart is still occurring
myocytes are no longer responding due to their impaired function c
tissue hypoxia.

Hypoxia: Hypoxia occurs when the tissues arent getting enough ox

Reasons for this can be decreased perfusion to the tissues, low oxyg
levels in the blood stream, or lack of blood flow to the area. The tis
need oxygen to survive and function properly. When there is a lack
oxygen, the cellular metabolism is altered. If there is altered cellula
metabolism in tissues of the heart, the heart cant pump effectively
decreased oxygen levels, the myocytes arent receiving the nutritio
need to allow for contractures to help pump blood from the heart. T
will physically stop beating although there is still the electrical stimu
The electrical activity is still stimulating the heart to beat, but becau
the altered cellular metabolism, the myocytes cant respond to the
activity.

Hypokalemia/Hyperkalemia: The heart requires a delicate balance o

potassium and other electrolytes to function properly. Potassium is
helping maintain the resting membrane potential of a cell. If there
potassium levels, it takes a greater force to change the resting mem
potential of the cell into an action potential. This means that the no
electrical stimulation for the SA/AV nodes of the heart is no longer a
enough stimulation to change the resting membrane potential to ca
action potential. The heart will no longer respond to the stimulation
wont beat even though the electrical activity is still moving through
heart. If there are low potassium levels, it takes a smaller force to c
the resting membrane potential and repolarization may never fully
(Lederer et al., 2015). The stimulation from the SA/AV node now be
too large of a stimulation causing the membrane to be easily chang
action potential and preventing the cell membrane from being resto
repolarized, resting potential phase. The fact that the membrane d
repolarize to a resting potential phase makes the following SA/AV no
stimulations ineffective. If the membrane is already in an action po
state, any stimulation to bring it from a resting potential to an actio
potential phase will serve no purpose. The heart is frozen in an act

Rebecca Sopelak

potential (contracture) state due to its inability to repolarize. Ther

electrical activity occurring to try to change the resting potential to
action potential, but there is no resting potential for the electrical
stimulation to work on.

Hypothermia: Hypothermia occurs in patients who has a accelerate

heat combined with a decreased production of heat. When hypothe
occurs, it decreases the heart rate in an effort to decrease heat loss
602). It also slows down a patients metabolic rate to maintain ene
other necessary life functions (Sole, 602). When a patient is hypoth
the whole body slows down to try to conserve energy and preserve
slowed heart rate, the patient is having a decreased cardiac output.
decrease in cardiac output decreases the tissue perfusion in the bod
can lead to a decreased cellular metabolism. The decreased cellula
metabolism is what leads to the inability of myocytes to function pr
With a decrease in metabolic rate, nutrients arent being broken dow
absorbed into the bloodstream, which also affects the cellular meta
by causing an imbalance in electrolytes. The electrolyte imbalance
cellular metabolism alteration will slowly cause the myocytes to shu
and become unresponsive. Electrical activity will still be trying to st
the myocytes, but with a decrease in the vital nutrients, they wont
energy and nutrients to respond to the stimulation.

Tension pneumothorax: When an injury occurs that results in a tens

pneumothorax, the patient has air leaking into the pleural space. A
patient continues to breath, the air begins to build up in the pleural
The more air the builds up in the pleural space, the more pressure t
builds in the intrathoracic cavity. This pressure compresses the hea
making it unable to beat (Sole, 603). The signals from the electrica
of the heart are still firing, but the external compression from the in
intrathoracic space is preventing the heart from moving and beating
the problem is fixed, via needle thoracostomy, the heart will have th
to beat again.

Cardiac tamponade: A cardiac tamponade occurs when blood fills in

pericardium. The pressure that builds up as more blood pools in the
pericardium puts pressure on the heart. If the pericardium has too
blood in it, it becomes stiff and can no longer expand. If the pericar
cant expand, the heart has a limited space to move around in prev
from being able to pump effectively. As the blood continues to pool
pressure continues to build up, the heart no longer has space to go
expand with diastole. The pressure will cause the heart to stop bea
although there is still electricity going through the heart. The heart

Rebecca Sopelak

beat again once the pressure is gone and there is room for the hear
expand and move around in again. The way to treat this would be t
pericardialcentesis to draw the blood off from around the heart. Th
be signs of electrical activity on an EKG because there are still elect
currents running through the heart to try to allow it to pump, there
room for the heart to move so it is currently stuck at a standstill.

Toxins: Overdoses can have a variety of reasons as to why a PEA ma

Depending on the symptoms that the patient has and what drug the
overdosed on can cause a variety of reasons for a PEA. For some pa
overdose causes respiratory distress from a severe decrease in resp
(Drug overdose: symptoms, 2014). This respiratory distress decrea
oxygen getting into the lungs thus decreasing the oxygenation of th
This decrease in oxygenation leads to a tissue hypoxia, thus causing
altered cellular metabolism. The altered cellular metabolism leads
inability of the myocytes to function properly and respond to electri
stimulation. For some patients, overdose induces vomiting and diar
(Drug overdose: symptoms, 2014). Vomiting and diarrhea causes a
decrease in potassium levels. If the potassium levels decrease too
can cause hypokalemia. As discussed in the hypokalemia discussio
creates a larger force needed to change the cell membrane resting
to an action potential. The SA/AV node are no longer a strong enou
to stimulate the change in the resting potential to an action potenti
causing no response by the heart even though there is still electrica
For some patients, the drug that the person overdosed on can caus
bleeding (Drug overdose: symptoms, 2014). This bleeding, if not ca
early, can cause hypovolemia. You then get the same situation you
with a hypovolemic patient where they have a temporary response
RAAS system and baroreceptors, which eventually wear off and cau
decrease in cardiac output, a decrease in tissue perfusion, an altera
cellular metabolism, and an inability of the myocytes to properly res
the electrical stimulation. In all three of these instances, the alterat
cellular metabolism, whether from electrolyte imbalances or oxygen
problems, there is an inability for the myocytes to respond to the el
stimulation. The myocytes dont change and cause contractures, e
though there is still electrical activity occurring to try to stimulate th
myocytes.

Pulmonary thrombosis: A pulmonary thrombosis is a blockage of an

the heart by a clot. The problem that occurs with this is that if the b
gets to be large enough to clamp off the artery, no blood can flow a
this. This will then cause a back up of blood flow in the artery. The
that runs through the lungs comes from the heart. It the blood flow

Rebecca Sopelak

backed up near the artery, it continues to build. Over time, the bloo
get backed up into the heart. With the blockage in the lung, the he
nowhere to send blood from the right side of the heart. It will begin
right side, causing increased pressure, increased amount of blood a
further back up of blood flow due to the inability of the heart to ejec
into the pulmonary circulation and receive blood from the body. Se
the heart can no longer send blood into the pulmonary circulation d
blockage in the pulmonary circulation and the accumulation of bloo
increasing the pressure inside the heart, the heart can no longer sq
down to allow blood out of the right side of the heart. The left side
heart becomes virtually empty. Some small amounts of blood may
to squeeze past the blockage, but without adequate blood flow gett
the clot in the pulmonary there isnt much blood to be returned from
lungs to the left side of the heart to put into circulation. Without thi
the oxygenated blood volume in the body will decrease, thus leadin
hypoxia of tissues. With the increase in pressure on the right side a
decrease in blood volume on the left side, the heart can no longer s
blood out of it causing tension and a stoppage of the heart. There w
be electrical impulses because the nodes are still firing to try to get
heart to pump, but there is nowhere for the blood to flow causing in
pressure and build up of blood in the heart. The way to treat this is
resolve the clot in the lungs to allow for blood to flow through the ve
again.

Coronary thrombosis: Similar to a pulmonary thrombosis, a coronar

thrombosis is a clot that blocks a coronary artery. It also causes a b
of blood flow into the heart. The back flow causes an increased pre
with no where for the blood to go. As more blood begins to pool, th
ability to contract and eject blood from the heart decreases thus res
a decreased cardiac output and ejection fracture. This then decreas
amount of perfusion getting to the tissues. With the decreased tiss
perfusion comes tissue hypoxia causing an altered cellular metabol
alteration in cellular metabolism causes the myocytes to not be abl
function properly. The electrical activity is still in take, but the due
pressure of the blood building up in the heart, the altered cellular
metabolism, and nowhere for the blood to be ejected to, the heart c
respond to the electrical activity that is stimulating it.

Rebecca Sopelak

References:

Drug overdose: Symptoms. (2014). Better Health Channel: Victoria State

Government. Retrieved from
https://www.betterhealth.vic.gov.au/health/healthyliving/drug-overdo

Lederer, E., Nayak, V., Alsaukas, Z.C., Bautman, V., (2015). Hyperkalemia: pathophysiology. M
Retrieved from: http://emedicine.medscape.com/article/240903-overview#a4

Sole, M.L., Klien, D.G., Moseley, M.J., (2013). Hypovolemic shock: Figure 11Critical Care Nursing, Sixth Edition. 273.

Sole, M.L., Klien, D.G., Moseley, M.J., (2013). Electrical therapy: Defibrillatio
Automated External Defibrillation. Critical Care Nursing, Sixth Edition
232.
Sole, M.L., Klien, D.G., Moseley, M.J., (2013). Exposure and environmental
considerations. Critical Care Nursing, Sixth Edition. 602.

Sole, M.L., Klien, D.G., Moseley, M.J., (2013). Assessment and management
specific organ injuries: Tension pneumothorax. Critical Care Nursing,
Edition. 603.

Sole, M.L., Klien, D.G., Moseley, M.J., (2013). Therapeutic hypothermia after
arrest. Critical Care Nursing, Sixth Edition. 244-245.