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ART MATRIX A MODEL FOR INPATIENT CARDIAC ARREST

INTRODUCTION

The University of California San Diego (UCSD) Medical Center has developed
its own version of advanced cardiac life support (ACLS). Known as ART, short for
Advanced Resuscitation Training, this innovative resuscitation training program
has had a significant impact on outcomes. Since its implementation in 2007,
the incidence of cardiac arrest is down, and the survival-to-discharge rate among
patients who do suffer cardiac arrest is approaching 50%. Furthermore, UCSD
Medical Center has seen a significant drop in overall mortality since ART was
instituted. Data shows that more than 300 deaths are prevented each year thanks
to ART.

The first tenet of this program is to prevent the preventable. The ART team has
been very proactive in this regard, using continuous quality improvement data to
identify problem areas and implement changes to address them. The ART Matrix
they have created helps staff understand the various etiologies of inpatient arrest
and establish the best approaches to preventing each kind. This matrix and the
ART algorithm are an essential part of ART training at UCSD, which also focuses
on the other two tenets of the program: resuscitate the resuscitatable and recognize
the futile.

This booklet is based on a presentation by Sheri Villanueva-Reiakvam, an ICU


critical care nurse at UCSD. Ms. Villanueva-Reiakvam, who works as a code nurse
and a rapid response nurse, is one of the people responsible for training code nurses
CPR Island
At UCSD, we do not take American Heart Association advanced resuscitation
classes. We have our own unique algorithm. We apply our own cutting-edge
resuscitation science to the inpatient population. And we call it Advanced
Resuscitation Training. ART has three primary goals:

• To prevent the preventable


• To resuscitate the resuscitatable
• To recognize the futile

This is our basic algorithm (see Figure 1). It’s a two-sided card. That’s it. We keep
it simple. One side is the “perfusing” side (Side A). The other side is the “non-
perfusing” side (Side B)—what we call the “dead” side.

How do you know if the patient is dead or alive? Simply by determining if they are
breathing or not. If a patient has a witnessed V-fib [ventricular fibrillation] arrest,
we start compressions and defibrillate three times right off the bat. If the arrest is
not witnessed or the rhythm is not VF or VT [ventricular tachycardia], we go to
something called CPR Island (see Figure 1 Side B). CPR Island is used to teach our
code members to remember how to get every step of the code. We want them to be
masters of these five questions:

• Is the patient dead?


• Are good chest compressions being performed?
• Are good ventilations being performed?
• Has a pressor been given?
• What does the monitor show? Is the rhythm shockable or do you
see signs of perfusion?

If the patient has a shockable rhythm, we are going to shock. If it’s not shockable,
what does the monitor tell us? Is this person showing signs of ROSC (return of
spontaneous circulation) or signs of perfusion? For example, is end-tidal CO2
greater than 20? Is the heart rate greater than 40? Do you see simultaneous pulse
oximetry waveforms going along with the ECG QRSs? During the code, we just
keep reviewing the steps on CPR Island.

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Figure 1
The ART algorithm – Side A

2013 UCSD ART/PART* PERFUSING PATIENT ALGORITHM

•  Determine perfusing status


•  Support airway (oxygen, “shark hook”, NPA/OPA, advanced airway)
•  Obtain vital signs
•  Ensure vascular access
•  Monitor (consider placing defibrillator pads), consider ECG

Circulation Issue Ventilation Issue Dysrhythmia Neurological Issue


Hermorrhage control Oxygen Supine (watch airway) Oxygen, fluids
Supine (watch airway) Upright position Place defib pads Check glucose
Fluid bolus, blood Assisted BVM Prep defibrillator for Consider Narcan
Pressors Consider Narcan pacing/cardioversion Stroke Code?

Tachycardia Symptomatic Bradycardia


(assure rhythm is primary cause of symptoms)1 (assure bradycardia is not due to hypoxia)2

Stable Unstable

Medications Cardioversion Atropine 0.5 mg IV


SVT (narrower, reg) • Set to Sync Mode
•  Adenosine 3
• Energy settings same
A-fib/flutter (irreg) as defibrillation4
•  Diltiazem3 • Consider sedation
No
Response
V-tach (wider, reg) • Confirm Sync Mode Response
•  Amiodarone3 before each shock

Medications Pacing
• Atropine boluses3 • Set to “Pacing”
• Pressor infusion • Confirm rate = 82/min
(epinephrine, dopamine)5 • Titrate mA until capture

*PART: Pediatric Advanced Resuscitation Training

Dysrhythmia more likely with: sudden change in rate, change in morphology or wide complexes, faster rates
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(HR>150 aduts, HR>180 children, HR>220 infants)


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Heart rate will begin to slow with SpO2 <70-80%, in which case oxygen is correct therapy

Adenosine (6mg-12mg adults; 0.1mg/kg-0.2mg/kg peds); diltiazem (10-20mg adults); amiodarone (150mg
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adults; 5mg/kg peds); atropine (0.5mg-1mg adults; 0.02mg/kg peds)


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120J-150J-200J (2J/kg-4J/kg-4J/kg peds; initial cardioversion attempt at 1J/kg also acceptable)
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Epinephrine (1-10 mcg/min adults; 0.01mg/kg q3” peds); dopamine (5-20 mcg/kg/min adults)

Copyright ©2012 UC Regents


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Side B

2013 UCSD ART/PART ARREST ALGORITHM

Initial Assessment
Monitored VF/VT arrest IF ARREST1, THEN START COMPRESSIONS2
Not VF/VT
Defibrillate3 ASAP OR
CPR Island
(repeat x 2) Unmonitored

CPR
•  Compressions2
•  Ventilations4
•  Pressors
•  Vasopressin (ADULT)5
•  Epinephrine5 }
May alternate every 3 min
•  Monitor
•  Shockable rhythm or signs of perfusion (ECG, EtCO2, SpO2)

Reversible cause of arrest?6

HR>40
VF/VT (HR>60 younger children) No perfusion
AND EtCO2>20

Defibrillate Perfusion Check (<10 sec)


• Administer pressor (if not recently given) • Pulse check
• 2 min CPR Shock3 Immediate CPR • Sustained EtCO2 without compressions
• If persists/recurs, amiodarone5 • ECG-SpO2 concordance

Perfusion

Post-Arrest Care
• Maintain ventilations (EtCO2 ~35 mmHg)
• Adjust FiO2 to keep SpO2 95-98%
• Hemodynamic support/fluids
• Consider hypothermia

Unresponsive + apneic/gasping (+/- pulseless) OR VF/asystole OR HR<30 (HR<60 younger children) OR


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sudden HR/EtCO2
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Continuous compressions; 2+ inches (1/3 AP diameter in children), 80-120/min, full recoil
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120J-150J-200J (2J/kg-4J/kg-4J/kg peds), minimal pause in compressions before/after shocks

Synchronous (10:1) with continuous compressions (no pause); two rescuers; “two-thumbs-up” mask hold;
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consider OPA/NPA/cricoid pressure; intubate (min compression pause) when possible

Vasopressin (40U adults); epinephrine (1mg adults; 0.01mg/kg (0.1mg/kg ET) peds); amiodarone 300mg-
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150mg adults; 5mg/kg-5mg/kg-5mg/kg peds); atropine (1mg adults; 0.02mg/kg peds)

Hypovolemia (IVF/blood); hyper-K+ (NaHCO3, CaCI2); hypoglycemia (D50); acidosis (NaHCO3); PE (TPA);
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tension pneumothorax (needle); vagal (atropine); hypothermia (warming); recurrent VF (PCI)

Copyright ©2012 UC Regents


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Don’t stop
When it comes to chest compressions, in our algorithm, we don’t take breaks for
anything. We do continuous chest compressions from the time of cardiopulmonary
arrest until, hopefully, ROSC is achieved. We don’t stop to ventilate. We don’t stop
to intubate. We’ve taught our anesthesiologists to intubate while chest compressions
are going on. If the airway is the primary problem, we may stop chest compressions
for five seconds, but we all know that doing continuous chest compressions is more
vital than getting the oxygenation and ventilation on board.

I tell our people to really concentrate on the quality of their CPR. You need to push
all the way down until you hit solid organ and bone, and come all the way off the
chest and then all the way back down again. We don’t have a magic rate or depth,
so we say to go as fast as you can and as deep as you can for as long as you can—as
long as you have recoil. To allow for recoil, you have to make sure you come all the
way off the chest so that the chest returns to its original position. The reason that
this is so important is related to coronary perfusion pressure. We have to maintain
perfusion within the heart and make sure that the pump is full. And we want to be
sure that electrical activity is most prominent when the pump is primed.

When we do need to shock a patient, we keep pre- and post-shock pauses to a


minimum. We keep doing chest compressions while we charge the machine. When
you hear the beep, everyone wants to jump off, right? But we don’t do that because
we know how important it is to maintain coronary perfusion pressure. Once the
machine is ready, I say, “Is everyone clear?” I see that everyone is off the chest and
the shock is delivered. The pause is only three to five seconds, then back to CPR. If
your team is really proficient, you can do a lot to improve survivability by limiting
pre-shock and post-shock pauses.

Master the questions


Let’s review the questions. Question 1: Is the person dead or alive? How are
you going to know? Simply open the airway and see if they take a breath. In
our algorithm, if the person doesn’t take a breath, we immediately start chest
compressions because this patient is dead. They’re not breathing, so we’re not going
to check for a pulse. We’re not going to assume that they could be alive. When in
doubt, do chest compressions. If they’re alive, they will tell you because they will
start moaning.

Next question: Do we have good chest compressions? So what do good


compressions look like? As fast as you can, as deep as you can, as long as you’re
maintaining good recoil.
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The third question you’re going to ask yourself: Are good ventilations being
performed? In our algorithm, we deliver one breath every tenth compression, and
we do it on recoil. So this means that if you’re bagging a patient, you make sure
their airway is patent. We put in an oral airway because that’s how we also ensure
oral patency, and we have somebody squeeze the bag once every tenth compression
on recoil. It prevents you from hyperventilating the patient because all you’re doing
is watching the chest compressions. This allows for continuous chest compressions,
so we don’t have to stop CPR in order to deliver a breath.

The fourth question to ask: Has a pressor been given? In our hospital, the pressors
that we administer are 1mg of epi [epinephrine] every three to five minutes and
then 40 units of vaso [vasopressin]. So we’ll alternate vaso, epi, vaso, epi. We don’t
have a max on vaso. The reason being that the scientific data behind vasopressin
shows that it does not lose its efficacy in an acidotic patient, and we know that the
longer a person has CPR, the more acidotic that patient becomes.

And the last question: Is it a shockable rhythm? Is it time to dial up a shock, or


do you see signs of perfusion? As I mentioned before, signs of perfusion in our
algorithm are end-tidal CO2 of greater than 20. Heart rate is going to be greater
than 40. You’re going to see an ECG rhythm with QRS complexes and that should
hopefully correlate with a pulse oximetry waveform.

The Matrix
When you break down the etiologies of cardiac arrest, it’s eye opening. This is
where the ART Matrix comes in. The ART Matrix has three major objectives:

• To understand the various etiologies of inpatient arrest


• To consider the optimal strategy to address each etiology using the ART
approaches of prevention, resuscitation, and futility
• To review examples for the major causes of inpatient arrest, including
apnea, sepsis, and VF-related arrest

In the hospital setting, we see a whole slew of cardiac arrest etiologies. In our
hospital, we realized that we were focusing on V-fib and V-tac, but the reality is
that our patients weren’t dying from that. They were actually arresting from non-
intubated respiratory issues, which may sound familiar (see Figure 2). It could be
pulmonary disease progression, or maybe it’s tracheotomy related. Neurological
issues are another possibility. How many times have you had a patient who looks

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stable, and then all of a sudden they spike a temperature, followed by tachycardia
and shortness of breath within an hour or two. The patient looks normal and then
all of a sudden, they’re crashing—maybe because of a PE [pulmonary embolism] or
hemorrhage as a result of trauma.

Figure 2
Causes of cardiac arrest at UCSD
It’s as if the patient is
Unknown falling off a cliff. One
Sepsis vital sign indicates that
Non-intubated
respiratory your patient is getting
Hemorrhage short of breath. They
start breathing really
Pulmonary embolus fast. Their SpO2 starts
Heart failure
dropping, and what do
you see following shortly
VF/PVT
thereafter? Bradycardia.
All of a sudden they’re
Vagal/block going bradycardic, and
Intubated
respiratory Neurological you see their sats desat
and get lower and lower.
Then they’re in PEA [pulseless electrical activity], and you’re calling a Code Blue.
This is what we refer to as falling off the cliff.

Shockable Dysrhythmias
So let’s talk about the specifics of these etiologies. We’ve all seen patients who are
in the hospital because of a STEMI [ST-elevation myocardial infarction]. They
look stable and you’re trying to get them to the cath lab, and suddenly they go into
cardiac arrest. So at UCSD, we view these patients as really high risk V-fib Code
Blue patients, and we focus on helping our staff prevent this from happening. This
consists of simple steps such as making sure the patient has defibrillator pads on. Is
there access to the patient if the person does go into cardiac arrest, and are we ready
to give them the code drugs?

In my hospital, when a patient has V-fib or V-tach arrest, has pads on, and is
connected to a defibrillator, we actually do “stacked” shocks. We deliver three
shocks—boom, boom, boom—because the heart is primed, and should be most
receptive right at the very beginning. If a patient has witnessed V-fib while on
telemetry but doesn’t have pads in place, we do compressions first and then stacked
shocks. When a patient who is not on a monitor experiences V-fib, we would

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Figure 3
Survival to discharge for patients with VF or VT arrest

VF/VT
100
do two minutes of CPR,
90
administer a pressor, and
Survival to Discharge (%)

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then administer the shock.
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So does this work? The
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answer is yes. In 2008, we
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eliminated the stacked shocks
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from our algorithm, and we
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saw survivability from V-fib
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shocks, survivability for
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Presented at Resuscitation Science Symposium, 2012


arrest started climbing back up
(see Figure 3).

We now know it’s more important to get the shocks on board than it is to do CPR
for witnessed V-fib arrest. So in the outpatient setting, you can start with CPR, but
on the inpatient side, we’ve got defibrillators right there. Put the pads on and get
that machine charged up as soon as possible. If V-fib occurs within a code itself, we
tell our people: one shock at a time, then one pressor, and two minutes of CPR.
It’s pretty simple.

An ounce of prevention
In our hospital, we saw that patients were coming off telemetry to use the bedside
commode. We know it’s really uncomfortable for patients to be wearing all of this
stuff while they go to the bathroom, but when you sit on a Code Blue committee
and evaluate all of the codes and rapid responses, you see how many vasovagal
events are related to somebody getting out of bed to use the bathroom. The only
way to prevent this is to take small but important steps: Taking the blood pressure.
Sitting for two minutes before standing. Giving the patient a minute before you
expect them to go to the bathroom. And simple prophylactic measures like giving
patients stool softeners can really affect whether or not that patient is going to have
a vasovagal event. That’s the prophylactic side. But if a patient is vagaling, we have
atropine at the bedside. We actually took atropine out of the ART algorithm, so this
is the only time we use atropine now.

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Figure 4
Arrest-related deaths among septic patients Code Sepsis
SEPSIS
When it comes to sepsis
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Arrest-Related Deaths (per 1000 discharges)

prevention, I really believe


1.8
that nurse empowerment
1.6
is where it starts. With
1.4
1.2
sepsis, nurses are the
1 first line of defense. We
0.8 started a Code Sepsis
0.6 protocol within our ED
0.4 [emergency department]
0.2 and use the same protocol
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improvement] data showed


Presented at Resuscitation Science Symposium, 2012 that once somebody
who was in septic shock
coded, we could not bring them back—even with all of the medical technology we
have. We have to get in on the early end and prevent them from going into shock
in the first place. Under our sepsis protocol, you call the rapid response nurse,
who implements the process of getting chest X-rays, starting fluids, and getting
cultures done at the bedside. In addition, we have bundles of antibiotics for septic
patients that are ready to be pulled and mixed by our pharmacy. Since putting this
Code Sepsis bundle in place in 2011, we’ve seen a drop in cardiac arrests among
inpatients (see Figure 4). In addition, we need to have strong discussions with
the family when a patient is in septic shock. We talk to them about changing the
patient’s code status. This is when discussing futility on the early end is needed.

Staying up to date with current science can increase survivability for your patients.
For example, with hemorrhagic patients, vasopressin is the primary drug of choice
because studies have shown that perfusion is better and that patients respond better
than with epinephrine.

Respiratory interventions work


Ventilation is the big-ticket item. We knew that our patients were dying from
intubated and non-intubated respiratory issues, so we instituted a number of
respiratory interventions. For example, our Code Blue committee changed our
protocol so that patients on BiPAP [bilevel positive airway pressure] are no longer
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allowed on the progressive-care units. We realized that these patients were actually
in respiratory distress while on an intermediate unit but that the intervention just
wasn’t quick enough or aggressive enough. Now these patients are moved straight
to the ICU because chances are they will probably need to be intubated within the
next 24 hours, and we want to keep a close eye on them. It’s labor intensive and
bed availability in the ICU is an issue. But the reality is that it has changed our
outcomes. We want safety to be our number one priority.

Another change relates to patients who are on a ventilator during CPR. The
thinking was that if someone is on a ventilator, they’re obviously being ventilated as
best as they can. But based on our data, we knew it was better to Ambu bag them
because you can actually time when the breaths are being delivered in correlation
with the CPR. This has also improved our outcomes. You just have to look at your
data and see what it says.

Figure 5 Apnea awareness


The impact of apnea monitoring on respiratory arrests A lot of our patients have
RESPIRATORY ARRESTS/TOTAL ARRESTS sleep apnea, and when we
70 give them narcotics and other
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medications, we can make
the apnea worse and put
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them at higher risk of coding.
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Percent

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recognizes that this is an
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issue, we take precautions.
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taught our intermediate-care


Presented at American Association of Respiratory Care, 2012
nurses to look for signs and
major events that indicate a
patient has apnea. For example, the patient’s O2 sats might drop during their apnic
event, or they become bradycardic. We want to keep the death trap—the tongue—
from blocking the airway. Simply by rolling them over or opening that airway,
we can literally remove the tongue from blocking that 2-centimeter area. After
implementing this monitoring program, the percentage of respiratory arrests related
to apnea has dropped to about 30% (see Figure 5).
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Figure 6 EtCO2 vigilance
Cardiac arrest incidence by etiology We’ve put a lot of
3 work into end-tidal
Arrest Incidence (per 1000 discharges)

VF/VT
Vagal/block
CO2 monitoring and
2.5
Sepsis recognizing patterns.
Hemorrhage
2 CHF Someone who is in
PE
Respiratory
respiratory distress or
1.5
fatigue will show evidence
1 of fast rate, shallow
0.5
breaths, and low end-tidal
CO2. Somebody who’s
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Presented at Resuscitation Science Symposium, 2012
patient with respiratory
insufficiency is going to
have high end-tidal CO2 and will need to take deep breaths with full exhale. With
all three of these categories, we are probably looking at someone who needs to be
intubated or who needs very aggressive respiratory interventions. In addition, fast
breaths may indicate a patient with metabolic acidosis, who is compensating by
“blowing off ” CO2, which should produce a low end-tidal CO2.

Figure 7
Cardiac arrest-related deaths by etiology If you work in a teaching
2 hospital, you know that
Arrest-Related Deaths (per 1000 discharges)

1.8 VF/VT every July, we get new


Vagal/block
1.6 Sepsis interns and residents.
Hemorrhage After we implemented
1.4
CHF
1.2 PE ART in 2007 and started
Respiratory
1 tracking all of this data,
0.8 we noticed a pattern.
0.6 Every July, there was
0.4 a spike in medication
0.2 errors and narcotic-
0 related Code Blues. Once
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Presented at Resuscitation Science Symposium, 2012 interns how to avoid this
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before they even touched our floors, and the increase during July dropped.

We also started something called seated resuscitation. This is where you Ambu
bag a patient sitting up before they go into hypoxic events. An example would
be when you have a patient who’s in respiratory distress and you’re trying to get
them through while you’re waiting for anaesthesia to show up so that they can be
intubated. Previously when patients were in respiratory distress, we had been laying
them flat on their back, which was not helping them. It was hurting them. With
seated resuscitation, we actually help their respiratory drive—their diaphragm
muscles—give them that tidal volume for the extra three minutes that it might take
anaesthesia to get to them and intubate them effectively.

Our data showed that in our hospital, our patients were dying from intubated
respiratory or non-intubated respiratory issues. By identifying these issues and
teaching to them, as you can see, we’ve decreased the incidence of respiratory
issues and cardiac arrests altogether (see Figures 6 and 7).

You can see that we’ve seen a little rise in V-fib arrest. This is because we opened a
cardiovascular center, so we have a larger patient population with cardiac risk factors
that lead to V-fib arrest in acuity. We’ve also seen a bit of an upswing in vasovagal
events, so we are rolling out education on the topic of bedside commode use that
we hope will make a difference.

Figure 8
Arrest rates among ICU and non-ICU patients

4 Evaluating ART
Benchmark=3.7
Let’s look at the
3.5
benchmark for arrest-
Arrest Rate (per 1000 discharges)

ART
Benchmark=3.0
3 related deaths (see Figure
8). I really want you to
2.5 ART
notice that we’ve made the
2 biggest difference in the
non-ICU floors, simply
1.5
by giving our staff the
1 tools to intervene earlier.
ICU patients are really
0.5
sick, so it’s not likely that
0 we can prevent an arrest
Non-ICU ICU

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or change the outcome if patients do arrest. But in the non-ICU setting, there are a
lot of interventions that can be done, and that’s where we’ve made a huge difference
with ART training and education.

Our survivability from cardiac arrest to hospital discharge is in the 50% range,
which is probably one of the highest rates for any hospital ever (see Figure 9). And
since instituting ART, we’ve seen a drop in overall hospital mortality (see Figure 10).

Figure 9
Survival to discharge after cardiac arrest

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Survival to Discharge (%)

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Figure 10
Hospital Mortality

2.20
2.10
Hospital Mortality (%)

2.00
ART
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Figure 11
Prevented deaths at UCSD

350
DOA survival
300 ED prevented arrests
ED arrest survivors
ICU prevented arrests
Prevented Deaths (#)

250 ICU arrest survivors


Non-ICU prevented arrests
200 Non-ICU arrest survivors

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Preventing deaths is a crucial part of our program. As of 2012, we are approaching


the 350-deaths-prevented range (see Figure 11).

The ART algorithm is built around emerging science, patient needs, and new
technology. We do frequent training; our advanced critical care nurses are trained
yearly. Training is held monthly for all of our residents. During the training, we
focus on how we can prevent a code from happening, how to resuscitate the most
effectively if a patient does code, and recognizing when resuscitation is futile in
certain patient populations.

Our algorithm is built around emerging science, inpatient needs, and new
technology. Our resuscitation program not only helps to improve patient outcomes,
it prevents them from actually coding in the first place.

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Authored and presented by Sheri Villanueva-Reiakvam, RN

Printed in U.S.A. PN-287

©2014 ZOLL Medical Corporation. All rights reserved.