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CARDIAC ARREST
125
haven’t gotten control of their rhythm and blood pres-
sure right away, I think they should be pronounced.
DB: That’s the way clinical care has evolved. Our
codes are much shorter than they were when I fi rst
was on staff or in training 20 years ago.
PR: I think that’s reasonable. I believe this led us to the
high dose epinephrine, which was supposed to have
been the magic bullet breakthrough for cardiac arrest.
Then we discovered all it did was keep the patients
alive long enough to have a three-day stay in the
coronary care unit, and markedly increase the cost of
dying. Is there a drug that has enabled you to salvage
a patient in arrest? I am underwhelmed by the use of
the antidysrhythmic drugs. I don’t think amiodarone
or lidocaine have saved lives. Perhaps epinephrine has
converted a couple of people from fi ne VF into a VF
more amenable to defi brillation.
AM: The AHA guidelines from 2005 do admit that
there are no antidysrhythmic drugs that improve
survival to discharge, in contrast to 2000 when the
recommendations favored amiodarone. The 2005
guidelines express a similar sentiment toward the util-
ity of vasopressors.
6
PR: This patient who we presented today with
renal failure is part of a subset of cardiac arrest that
strangely, often, has a good outcome. I have been sur-
prised at how easily these patients resuscitate from
what’s most likely a hyperkalemic arrest, although
I’m also surprised at how often they go into arrest,
even when they are being regularly dialyzed.
EU: I think hyperkalemia is easier as an electrocardio-
graphic abnormality to correct, but I think that when
they arrest, these patients may perhaps be even more
diffi cult to fully resuscitate because there is always
extensive concomitant pathology present.
AM: Renal disease is associated with a very poor
prognosis in many conditions. Patients with strokes
and renal disease, patients with MIs and renal disease,
and patients with heart failure and renal disease all
have worse outcomes. It’s not the renal disease itself
that makes the cardiac arrest more intractable, but the
underlying other medical illnesses that makes the car-
diac arrest more intractable.
PR: Do you think that the standard antipotassium
pharmacologic therapy is indicated for the renal
These are the patients who we really might be able to
help. The likelihood of success in any cardiac arrest
depends on what is the underlying disease.
PR: When I started in medicine, we were taught to
respond to an arrest by opening the chest. Our results
weren’t as dismal as many of the results of patients
who arrive in the ED with VF or asystole, yet once
closed-chest defi brillation became widespread in use,
open chest resuscitation was reserved for patients who
already had their chest open. I’ve never understood
what the difference was, although perhaps direct
defi brillation works a little better than defi brillation
through the chest wall. I’ve always been puzzled as to
why those patients survived with open chest massage
when they don’t with closed.
SG: We are more leery of opening a chest today,
typically because of the risk it entails to the provider,
particularly if you are not used to opening the chest.
Risks can include blood and body fl uid exposure and
exposure to sharps, and the risks that the patient will
go through, such as infection and wound healing. In
addition, I am not aware of results that show that it’s
a better therapy.
DB: If you were in a community hospital and you
opened the chest and resuscitated the patient, what
would you do if you didn’t have a cardiothoracic sur-
geon there?
PR: I would not open the chest if you don’t have the
capacity to fi x the obstructed vessel; all you could do
is close the chest and hope that the patient survives,
which is what we were formerly doing because we
didn’t have the capacity to fi x the problem. The bypass
graft surgical techniques were just being developed,
so we just closed the chest and admitted the patient
to the medical service, with a surgical consultation to
manage the chest wound.
DB: I wonder if a lack of surgical resources is what
moved us towards closed-chest compression?
PR: I think this was more because there were fewer
people who knew how to open a chest, and it was much
easier to learn how to defi brillate. Unfortunately, it
was an excellent technologic improvement, but not an
excellent outcome improvement. I continue to wonder
what we could do to improve our results. We spend
too much time trying to resuscitate a patient with car-
diac arrest; if they don’t defi brillate right away and you
CHAPTER 9
126
PR: One of the things that always used to irritate me
when I practiced in San Diego was our helicopter
being called for a large number of cardiac arrests. It
seemed to me that was a dreadful misuse of the heli-
copter. I never could understand why those patients
couldn’t be pronounced dead on site. I would won-
der if it isn’t time that we stop racing cardiac arrest
patients through the streets in ambulances. I would
consider pronouncing patients in the fi eld, if they
could not be defi brillated immediately.
AM: I think that we should probably be more will-
ing to pronounce patients in the fi eld. Transporting
with lights and sirens is associated with traffi c crashes
and dangers to the public as well as to the responders,
and the arrested patient is diffi cult to treat in a mov-
ing ambulance. There are studies that have looked
at reasonable indications to pronounce a patient in
the fi eld. Several years ago, the OPALS study group
proposed criteria for termination of prehospital resus-
citation for victims of cardiac arrest.
7
There are fi ve
different criteria, including event not witnessed by
EMS personnel, no shock in the prehospital setting,
no return to spontaneous circulation in the prehos-
pital system, event was not witnessed by a bystander,
and the bystanders did not administer CPR. Common
sense would dictate that, considering those fi ve criteria
together, there is no way a person is going to survive
to discharge. Unfortunately, the prehospital medical
directors often have tried to employ these rules, but
their responders frequently will not follow them and
transport the patient in any event.
I think that the prehospital care providers often
times feel a lot of pressure pronouncing the patient in
the fi eld when the family is hovering over them, yell-
ing at them, “Please do something!” It’s a lot harder
to convince the family in the fi eld that the patient
has no chance of survival. In addition, I think that a
big problem we have in our society is that we have a
tremendous societal expectation or misperception of
resuscitation rates. Society really thinks that people
who are in cardiac arrest who are getting CPR are
probably going to survive. This may be related to the
media, but I don’t think the public has any concept
that the chance that a patient will survive a prehospi-
tal arrest is, at best, 5%.
PR: We had a few rules for withholding resuscita-
tion that we added in Denver, including decapitation,
decomposition, and rigor mortis on a warm night.
failure patient who arrests? Would you start them all
on insulin and bicarbonate and calcium?
DB: I think that, in this particular case, the likelihood
is that the patient is having ischemic cardiac arrest.
My experience with hyperkalemic arrest is that these
patients don’t have abrupt VT; instead, they tend to
sequentially peak their T waves, broaden out their
PR interval, lose their P waves, and then fi nally
broaden out their QRS in a slow, sinusoidal, bradya-
systolic arrest. I fi nd those patients easier to resusci-
tate because one generally has more time while they
are getting worse. If you catch the very end, then
resuscitation can be more diffi cult. Calcium chloride
is very effective if you catch hyperkalemic dysrh-
thymias early. A patient who presents with abrupt
VT like this patient, in the setting of a STEMI, is
unlikely to also have acute hyperkalemia causing the
arrest. In this patient I probably wouldn’t reach for
antihyperkalemic therapy. Instead, I would look to
shock this patient, move to the catheterization labo-
ratory as soon as possible for revascularization, and
at the same time cool the patient as much as I could
while I’m waiting.
AM: If the patient were refractory to therapy, then I
would consider treating this patient for acute hyper-
kalemia with calcium and bicarbonate, and then all
the other appropriate hyperkalemia therapies.
PR: One area that causes dysrhythmic arrest that we
used to see more frequently is digitalis toxicity. I used
to think that virtually all patients we saw who came
in with dysrhythmias were digitoxic, but that seems
to be a lot less common today. Do you think they do
better if you have the opportunity to reach for Fab
fragments therapy?
AM: I think we are seeing fewer cardiac arrest. Fewer
and fewer patients are being treated with digoxin.
I’ve given Fab fragments to patients who were taking
digoxin and had life-threatening dysrhythmias, although
they were still perfusing, and I have witnessed dramatic
successes.
PR: Other severe electrolyte disturbances can also lead
to dysrhythmia. It seems like our treatment of hyper-
tension has helped us to see fewer arrest patients with
hypokalemia, since we’re not using thiazide diuretics
as much to treat hypertension. Yet, none seem to turn
around as magically as hyperkalemia.
CARDIAC ARREST
127
the rhythm is stabilized. Part of this problem involves
how to get the patient from the fi eld to a hospital that
has the catheterization laboratory. Given our ever
increasing hospital crowding, we simply are probably
losing some of these patients because we don’t have
open access to an institution that has a 24-hour cath-
eterization laboratory.
EU: In Boston, where it was initially studied, we are
bypassing the EDs that do not have a 24-hour catheter-
ization laboratory with patients with ST-elevation MIs.
8
When EMS calls ahead, and the paramedic has already
done a 12-lead EKG, the ED itself can call the catheter-
ization laboratory to open up. They will not go to a
hospital that does not have a catheterization laboratory.
I think that this model will likely generalize as we con-
tinue to show improved outcomes for these patients.
DB: In Massachusetts we also just abolished diversion
for all hospitals statewide, so that diversion should
no longer be an impediment to getting patients to the
right hospital.
Case resolution
Upon arrival to the ED, the patient had a repeat
cardiac arrest with a cardiac rhythm of pulseless
ventricular tachycardia. She received an immediate
defi brillation, and converted back to sinus tachycar-
dia (rate 110/minute). The EKG continued to dem-
onstrate the previously noted ST-segment changes.
Empiric calcium was administered via IV in the event
that she was hyperkalemic, though laboratory studies
later revealed a normal serum potassium value.
The patient met criteria for induced hypothermia
(unconscious with spontaneous circulation after
resuscitation from cardiac arrest), so she was intu-
bated, kept sedated, and paralyzed to prevent shiver-
ing. Cooling was initiated with cooling blankets and
cool IV fl uids. The cardiology service was consulted
emergently because of the EKG evidence of STEMI,
and 45 minutes after arrival she was transported to
the cardiac catheterization lab. A 100% right coronary
artery blockage was opened, and a stent was placed,
after which she was admitted to the coronary care
unit. Therapeutic hypothermia was discontinued after
approximately 18 hours, and the patient made a steady
improvement. She was discharged home 6 days later
with minimal cognitive defi cits, and was able to care
for herself independently. Outpatient occupational
therapy follow up was arranged. The family members
The one exception is pediatric arrests, which I believe
are better pronounced at the hospital, not because
they do better, but because the social requirements of
dealing with a pediatric death are such that it’s best to
start at the hospital.
PR: This particular patient was lucky in that she
probably survived the dysrhythmia at home; maybe
the efforts to do CPR were comparable to the cough
technique or doing a chest thump. The cough tech-
nique has been shown to be effi cacious as long as the
patient is still conscious and can institute the cough.
You can get people to do this as they’re suddenly
descending into a dysrhythmia, but it doesn’t work
once the patient has lost consciousness.
SG: Sometimes, the couple of joules of energy with
a chest thump may be all you need to convert an
early VT to sinus rhythm, and can save valuable time
wasted trying to employ a defi brillator.
PR: Perhaps we as emergency physicians are going to
feel even more futility in trying to resuscitate out-of-
hospital cardiac arrests, because now a number of high-
risk patients who have implanted defi brillators don’t
have cardiac arrests anymore; these were the patients
who would present with VT and VF amenable to defi -
brillation, and most likely to survive an out-of-hospital
cardiac arrest if they had access to defi brillation. With
these patients no longer part of the denominator, the
patients that we are seeing as emergency physicians
with out-of-hospital arrest are even more likely to have
heart rhythms that are not amenable to defi brillation,
and so they will be more likely to die.
AM: In addition, the growing number of people with
underlying heart disease placed on chronic beta-
blocker therapy has decreased signifi cantly the overall
incidence of VF cardiac arrest. Instead, we are see-
ing an increase in asystolic and PEA cardiac arrest.
Overall, we are probably seeing fewer cardiac arrests,
and the ones that we see are presenting with rhythms
that are not amenable to defi brillation.
PR: This case may ultimately be frustrating because
you think that you’ve had a salvage, but this is a
patient, given her comorbidities, who is probably not
going to survive in the hospital, and if she gets out of
the hospital, the chances are that her fi nal outcome
will be death. However, we must try to respond, keep-
ing in mind is that if this is an ischemic arrest, the
patient must go for an intervention very quickly once
CHAPTER 9
128
current research estimates that 50% of all deaths
from cardiovascular disease are sudden and unex-
pected, occurring shortly (instantaneous to 1 hour)
after the onset of symptoms. Predictably, data suggest
two peak ages of incidence for sudden cardiac death:
infants under 6 months comprise one peak, and the
other involves adults from 45–75 years of age. Most
sudden deaths occur outside of the hospital, and may
therefore remain unwitnessed.
9,15
The occurrence of sudden cardiac death heralds an
inexorable march towards global cellular destruction.
The neurologic disability among survivors is often
devastating, and patients may require varying types
of artifi cial life support to maintain vital functions.
Out-of-hospital cardiac arrest is associated with
low survival to hospital discharge (2–9%) and even
lower rates of functional neurologic recovery. Though
recent years have borne witness to an expansion of
resuscitation research, the emphasis still remains on
time-tested interventions such as: (1) bystander CPR,
(2) defi brillation, and (3) adequate compressions.
Current treatment recommendations will detail this
renewed “back to basics” focus.
16
Initial patient assessment
Brain death and irreversible neurologic dysfunction
begin within minutes of circulatory collapse; the like-
lihood of survival with a functional neurologic out-
come decreases with every minute that passes prior
to the initiation of resuscitative efforts. The treatment
of the patient in cardiac arrest should be focused on
the restoration and maintenance of perfusion. Return
of spontaneous circulation (ROSC) is most likely
in those patients who receive prompt bystander CPR,
technically adequate compressions, and rapid defi bril-
lation of a ventricular dysrhythmia.
10,14
Obtaining information about the events surround-
ing cardiovascular collapse is exceedingly diffi cult for
the emergency physician. Bystanders may give details
about resuscitative efforts, and emergency medical ser-
vices personnel may have valuable information about
the incident scene. The presence of pill bottles, for
example, prompts a consideration of toxic overdoses in
the initial differential diagnosis; alternatively, patients
transported from a nephrologist’s offi ce may have an
electrolyte derangement that precipitated a lethal dys-
rhythmia. With respect to pulseless electrical activity,
the consideration of toxidromes is vital to articulating
who performed chest compressions prior to paramedic
arrival can be credited with saving her life.
Section III: Concepts
Background
Cardiac arrest remains an expensive resource-inten-
sive condition that requires input from providers
across the disciplines of emergency medicine and criti-
cal care.
9
Survival from cardiac arrest remains poor
despite prolonged and extensive resuscitation research
initiatives. Despite revisions in prehospital treatment
protocols and an increased awareness among the
general public, this condition is still associated with
an extremely high mortality. Paramedics routinely
encounter cardiac arrest patients in the prehospital
setting, and emergency physicians are charged with
orchestrating initial resuscitative efforts.
Dismal rates of neurologic recovery from cardiac
arrest have encouraged continued and thoughtful
re examination of resuscitation strategies. Protocols
that minimize interruptions to chest compressions, and
focus on the maintenance of cerebral blood have gained
recent emphasis. The initial evaluation and stabiliza-
tion of the patient in cardiac arrest now focuses less
on pharmacology, and more on the mechanics of circu-
lation. Time tested modalities like defi brillation and
chest compression are reemerging as powerful tools in
the emergency physician’s resuscitative arsenal.
10,11
Cardiac arrest poses unique challenges to the deliv-
ery of emergency health care. Cardiac arrest is never
entirely predictable, but the survival clock starts ticking
once circulation ceases. Access to trained and willing
bystanders is not universal, and automated external
defi brillators may not be immediately available. The
inverse relationship between survival and time has
remained constant; consequently, meaningful neuro-
logic recovery is predicated upon the timely delivery of
chest compressions, and access to defi nitive care.
12–14
Epidemiology
In the United States, sudden cardiac death accounts
for approximately 200,000–400,000 deaths per year.
Precise statistics represent unique epidemiological
challenges because of subtle differences in the clas-
sifi cation of sudden death. Studies on sudden cardiac
death detail different inclusion criteria; nevertheless,
CARDIAC ARREST
129
confi rmatory techniques that can be rapidly per-
formed while minimizing any interruption in chest
compressions. Some paramedic systems have imple-
mented continuous carbon dioxide capnometry to
warn providers of inadvertent dislodgement. A rapid
respiratory assessment can also uncover potentially
reversible etiologies of cardiac arrest such as ten-
sion pneumothorax. Chest X-ray studies contribute
little information beyond what is discovered at the
patient’s bedside.
Heart tones are generally absent in cardiac arrest
patients, but the clinical examination can yield impor-
tant clues about contributing factors. The presence of
chest wall trauma may signal an underlying tampon-
ade. Patients with chronic renal failure and metastatic
disease harbor more subtle signs of tamponade, and
benefi t from bedside emergency echocardiography.
Utilizing the focused assessment for sonography in
trauma, or FAST window, emergency practitioners
can obtain a “quick look” at cardiac activity and
establish the presence or absence of a large pericar-
dial effusion (Figure 9-1). The parasternal long axis
represents an alternative and easily accessible cardiac
a comprehensive treatment plan. The initial history
must necessarily encompass relevant scene details, if
possible, and understanding of preceding events.
The absence of central pulses, respirations, and
responsiveness defi nes cardiac arrest. Agonal or gasp-
ing respirations may persist after the cessation of car-
diac activity, but effective breathing is absent during
circulatory collapse. Patients presenting to the ED
in cardiac arrest must be completely undressed. The
physical examination proceeds in a detailed but rapid
fashion. Priorities include airway maintenance, circula-
tory assessment, and an investigation for any potential
underlying causes of cardiac arrest. The history and
physical examination are performed concurrently with
resuscitative interventions.
Current recommendations place less of an empha-
sis on advanced airway techniques.
11,17
For patients
intubated prior to ED arrival, confi rmation of tube
placement is important, as movement of the patient’s
neck during transport or transfer has been implicated
in tube migration, and efforts should be directed at
verifi cation of tracheal location. Capnography, direct
laryngoscopy, and auscultation of lung sounds are
RA
LA
LV
RV
RA: Right Atrium
LA: Left Atrium
RV: Right Ventricule
LV: Left Ventricle
The bright, hyperechoic lining represents the pericardium. The dark and hypoechoic fluid
contained within the pericardial sac indicates a large effusion.
Figure 9.1 Schematic of FAST/
subxiphoid ultrasound window.
CHAPTER 9
130
compressions, and advanced life support providers
are encouraged to delay certain interventions if they
interfere with the delivery of chest compressions.
This shift in focus to BLS has particular relevance to
emergency medical services systems, as the majority
of advanced life support treatment (ALS) protocols
embrace the full scope of advanced cardiac life sup-
port. Previous resuscitation paradigms embraced
a drug-shock, drug-shock approach to life support,
and a large number of prehospital studies sought to
attribute survival benefi ts to one drug over another.
The widespread implementation of prehospital ALS
did not correlate with increased survival from car-
diac arrest. One of the largest prehospital studies,
the Ontario Prehospital Life Support (OPALS) initia-
tive, reports that paramedic-staffed EMS systems do
not convey any survival benefi t. In fact, better out-
comes are associated with BLS crews who are trained
in early defi brillation.
19
The renewed focus on BLS
techniques, coupled with data from studies similar in
spirit to OPALS, has produced a new approach to the
treatment of the patient in cardiac arrest.
“Push hard and push fast” captures the thrust of
newer resuscitation guidelines. The AHA advocates
window (Figure 9-2). Furthermore, ultrasound images
may complement performance of therapeutic pericar-
diocentesis. Similar to the respiratory assessment out-
lined above, bedside ultrasound complements ongoing
resuscitative efforts.
9,18
Basic life support (BLS) and out-of-hospital
cardiac arrest (OOHCA)
When the American Heart Association (AHA) detailed
its “chain of survival” metaphor, early CPR and early
defi brillation were featured components. Though the
chain also encompassed advanced care and interven-
tions, it remains clear that intact neurologic survival
is not possible without understanding basic life sup-
port as the foundation of effective treatment. Until
recently, the goal of survival from out-of-hospital car-
diac arrest has remained less than tangible. Intensive
resuscitation research and newer technology have not
been accompanied with complementary improve-
ments in patient outcome.
11
The document highlights the importance of mini-
mally interrupted compressions, compression-to-
ventilation ratios are changed to emphasize faster
AR: Aortic root and arch
RV: Right ventricle
LV: Left ventricle
LA: Left atrium
IW: Inferior wall of left ventricle
A: Apex
P: Pericardium
RV
A
P
AR
LA
LV
IW
Figure 9.2 Diagram of the
parasternal long axis in bedside
emergency echocardiography.
CARDIAC ARREST
131
model of cardiac arrest reveals that, “the genera-
tion of adequate cerebral and coronary perfusion
pressure” is the key to a good neurologic outcome.
The researchers confi rm that defi brillation is most
successful in the “electrical phase” of cardiac arrest,
which is thought to occur within the fi rst 5 minutes
following collapse. Not surprisingly, resuscitative
efforts begun during the “metabolic,” or third phase
of arrest, are not likely to result in success or mean-
ingful neurologic recovery.
22
Clearly, basic life sup-
port interventions have rightfully recaptured their
place at the forefront of cardiac arrest management.
Contemporary resuscitation paradigms must neces-
sarily advocate for early, rapid, and uninterrupted
cardiac compressions.
Advanced life support and emergency care
for cardiac arrest
The 2005 AHA guidelines for the management of
cardiac arrest begin with a reminder that drug ther-
apy and other advanced interventions are of “sec-
ondary importance” to BLS. The guidelines instruct
rescuers to “establish intravenous access, administer
any drug therapy, and insert an advanced airway”
after CPR and early defi brillation has been attempt-
ed.
11
A discussion of advanced life support in cardiac
arrest must begin with an acknowledgment that typi-
cal advanced cardiac life support (ACLS) strategies
have failed to show improvements in intact neuro-
logical survival.
Antidysrhythmics
Neurologically favorable outcomes do not corre-
late with newer drug therapies for cardiac arrest.
Several antidysrhythmic drugs that had been recom-
mended in the prior ACLS algorithms fail to confer
a survival benefi t. In 1999, an out-of-hospital trial
of amiodarone was reported to demonstrate a pos-
sible improvement in survival to admission; never-
theless, the benefi ts of amiodarone do not extend
to hospital discharge.
23
Rea et al. compared intra-
venous amiodarone to lidocaine for the treatment
of adults with pulseless ventricular dysrhythmias.
24
The patients treated with amiodarone exhibit a
decreased likelihood of survival, and no difference
can be detected in the number of patients alive in
the 24-hour period after cardiac arrest. Despite its
compression rates of at least 100 per minute that also
allow for full and complete chest recoil. Uninterrupted
compressions are thought to maintain a baseline
level of perfusion that is consistent with survival, and
EMS systems are now beginning to embrace this shift
back to basics. In his editorial on improving sur-
vival from out-of-hospital cardiac arrest, Eisenberg,
refl ecting on the 40th anniversary of out-of-hospital
cardiac care in 2006, notes the paucity of “dramatic
breakthroughs,” and affi rms that “there is ample evi-
dence that every minute saved in delivering CPR and
defi brillation translates directly into a higher sur-
vival rate.” Eisenberg encourages emergency prac-
titioners to focus on system-specifi c initiatives that
are designed to deliver CPR and defi brillator-capable
providers as fast as possible to the patient in cardiac
arrest.
16
Several landmark prehospital studies confi rm the
survival benefi t of a treatment algorithm that fea-
tures rapid compressions, and touts BLS interventions
as its corner stone. A large review by Ewy in 2008
examines the impact of newer treatment initiatives
started in Tucson, Arizona and in rural Wisconsin
communities.
20
Acknowledging the dismally low rate
of neurologically intact OOHCA survivors, several
medical directors collaborated to demonstrate the
impact of a push hard and push fast strategy. Called
“cardiocerebral resuscitation,” this subset of proto-
cols encompasses: (1) compression-only bystander
CPR, (2) minimally interrupted compressions, and
(3) modifi ed ALS protocols. Specifi cally, bystand-
ers are advised to initiate compressions at approxi-
mately 100 per minute. Paramedics delay intubation,
applying only passive oxygenation, until three series
of compression/defi brillation/chest compressions can
be completed. A retrospective study by Kellum and
Kennedy, et al.
14
details the results of such protocol
modifi cations. Neurologically intact survival follow-
ing OOHCA prior to the adoption of “cardiocerebral
CPR” was 15% (14/92). In the 3 years that followed
the implementation of newer guidelines, 39% of
patients (35/89) were neurologically intact.
Several physiological and practical principles
inspired these seemingly drastic alterations in the
treatment of OOHCA. First, a study conducted by
Valenzuela et al. notes that patients in cardiac arrest
do not receive compressions for approximately
50% of the time they are being actively treated by
paramedic personnel.
21
Second, a novel three-phase
CHAPTER 9
132
However, vasopressin does not have the adverse
beta-agonist effect of EPI, which is associated with
increased myocardial oxygen consumption. In theory,
therefore, vasopressin appeared to have the benefi cial
effects of EPI but without the drawbacks. Early stud-
ies utilizing a pig model for cardiac arrest appeared
to support to this idea.
42–45
These studies demonstrate
improved coronary perfusion pressure, improved
vital organ blood fl ow, improved cerebral oxygen
delivery, no increase in myocardial oxygen demand,
and improved return of spontaneous circulation.
However, other large studies failed to demonstrate a
survival benefi t or improvement in neurological out-
come among survivors, and so vasopressin cannot
be recommended as a preferred vasopressor.
46–48
The
2005 AHA guidelines also concede that, to date, no
vasopressor has demonstrated a survival advantage
to hospital discharge or improvement in neurological
outcome.
6
Specifi c clinical situations
Specifi c clinical situations mandate consideration
of alternative medications. Chronic alcoholics and
patients with congenital syndromes (Romano Ward,
Lown-Ganong-Levine) may exhibit conduction abnor-
malities on the routine or pre-arrest EKG. A specifi c
type of polymorphic ventricular tachycardia, tor-
sades de pointes, results from prolongation of the QT
interval. Patients presenting with torsades de pointes
require empiric treatment with magnesium sulfate,
though hemodynamic instability may demand elec-
trical countershock fi rst. Magnesium is commonly
administered as an IV push medication at a dose of
2–4 g. Magnesium has minimal side effects for the
patient in arrest, and has the potential to increase the
chances of successful cardioversion or defi brillation.
Patients who exhibit intermittent torsades de pointes
who are unresponsive to magnesium require overdrive
pacing with a pacemaker or isoproterenol.
Electrolyte abnormalities, such as hyperkalemia,
are extremely important to consider in the differen-
tial diagnosis of pulseless arrest. Patients with renal
insuffi ciency, diabetes, or hypertension may develop
dysrhythmias from altered cardiac repolarization.
Hyperkalemia may manifest in a wide variety of elec-
trocardiographic abnormalities. The hyperkalemic
patient in cardiac arrest may exhibit peaked T waves,
failure to capture, and a peculiar rhythm that appears
placement in several AHA algorithms, research fails
to corroborate the benefi ts attributed to amiodarone.
A retrospective case series that concluded in 2005
indicates that amiodarone does not effectively termi-
nate sustained monomorphic ventricular tachycar-
dia.
25
Procainamide has some utility in the treatment
of refractory ventricular fi brillation, and is favored
in other clinical scenarios (i.e., atrial fi brillation and
Wolff-Parkinson-White syndrome) because of its lack
of atrioventricular nodal blockade. The AHA cau-
tions rescuers to avoid multiple drug therapies, as
the chances of dysrhythmia and side effects increase
with each added medication. Overall, the preferred
and most time-tested therapies for pulseless ventricu-
lar dysrhythmias remain defi brillation and effective
cardiac compressions.
11
Vasopressors
Intermediate, escalating, and high dosages of epineph-
rine (HDE) had been given a class IIb classifi cation
(“possibly useful and effective”) in previous editions of
the AHA guidelines, largely based on animal studies
and small human trials.
26–33
These studies demonstrated
an improved ROSC and survival to hospital admission
when adult cardiac arrest patients are treated with HDE
versus standard dosages of epinephrine (SDE). It was
assumed that this improvement in ROSC and survival
to hospital admission would translate into increased
rates of survival to hospital discharge and neurologic
recovery as well. However, this was not the case.
Subsequent studies confi rm that HDE is not associated
with improved survival to hospital discharge, and there
is some evidence that HDE is actually associated with
a worse neurologic outcome in survivors.
34–40
No sub-
groups of cardiac arrest patients have been identifi ed
who benefi t from HDE, and, as a result, HDE is no
longer recommended.
In the 2000 AHA guidelines, the use of vasopres-
sin was incorporated as an alternative to the use of
epinephrine (EPI) in the protocols for cardiac arrest.
41
Vasopressin is a naturally occurring antidiuretic hor-
mone that acts upon receptors in the renal collecting
ducts, as well as upon receptors in vascular smooth
muscle. In high dosages, the vascular smooth muscle
effect produces potent peripheral vasoconstriction.
This results in the benefi cial effect of increased dia-
stolic aortic blood pressure and coronary perfusion
pressure, similar to the alpha-agonist effect of EPI.
CARDIAC ARREST
133
Post-cardiac arrest ED care: therapeutic
hypothermia and critical care interface
Arguably the most important recent intervention to
emerge out of contemporary postarrest resuscitation
research is that of therapeutic hypothermia (TH). The
history of therapeutic hypothermia dates back to its
use in cardiac surgery. Animal studies demonstrate a
survival benefi t, and the fi rst human trials for post-
arrest hypothermia by Bernard and colleagues took
place in 1997.
13
Conducted in Australia, the study
enrolled out-of-hospital victims of ventricular fi bril-
lation cardiac arrest. Of the 43 enrolled patients, 21
(49%) had a good outcome that was described as
“discharge to home or to a rehabilitation facility.”
13
A
multicenter European study confi rms clinical benefi t,
and the American Heart Association gives a class IIa
recommendation to induced hypothermia for victims
of ventricular fi brillation arrest.
11,13
Protocols for postarrest hypothermia are by no
means consistent. Some studies exclude rhythms other
than ventricular fi brillation, and cooling methods vary
according to hospital preference and resources. A 2006
study by Oddo et al. reports that the benefi ts of thera-
peutic hypothermia extrapolate to patients in hemor-
rhagic shock. This 2006 study enrolled patients with
all-cause cardiac arrest and describes hypothermia that
is initiated in the emergency department. Teams led by
critical care physicians “apply ice bags on the neck,
axillae, torso, and groin,” targeted to achieve a temper-
ature of 33°C. Other methods of inducing TH include
the application of cooling blankets, and the insertion
of specialized vascular catheters. Patients in the Oddo
et al. study underwent pulmonary artery catheteriza-
tion in order to continuously monitor core temperature
and had external cooling continued in the critical care
unit. The study demonstrates both survival and neuro-
logical benefi ts from cardiac arrest due to ventricular
fi brillation and shock. The benefi ts of therapeutic hypo-
thermia appear unrelated to the specifi c cooling method
(i.e., ice packs versus vascular devices). Any postarrest
hypothermia initiative must necessarily involve a coor-
dinated and multidisciplinary approach. Patients cooled
in the ED require defi nitive care in a critical care envi-
ronment that can monitor and maintain desired core
body temperature. Side effects from TH such as dys-
rhythmia and infection have been documented.
50,51
A
sample protocol for the initiation of hypothermia fol-
lowing cardiac arrest is detailed in Table 9-1.
as a “sine wave” pattern. Though these features may
not be readily apparent on a rhythm strip or pre-arrest
EKG, the diagnosis is often suggested from the patient
history. Patients transported from dialysis centers, for
example, are at high risk for hyperkalemia. Empiric
calcium gluconate or calcium chloride should be
administered if the diagnosis of hyperkalemia is prob-
able. Sodium bicarbonate may also be useful during
the initial resuscitation, but it is widely accepted that
calcium stabilizes irritable myocardial membranes,
and therefore has the most rapid onset of therapeutic
effect. Calcium precipitates in solution, so it should
not be given concurrently in the same intravenous line
as other resuscitation drugs.
Drug overdose is also known to cause cardiac arrest.
A full discussion of toxin-induced cardiac arrest is
beyond the scope of this chapter, but it is well-known
that AHA guidelines fall short in their treatment pro-
tocols when they are applied to patients with drug
overdose. Most of the usual antidysrhythmics have a
limited role in the treatment of cardiac arrest due to
toxic ingestion. Though not generally recommended
early in most protocols, the early consideration of
sodium bicarbonate, glucagon, and calcium should
be included in the early management of patients with
presumed drug overdose.
Sodium bicarbonate is the treatment of choice for
toxicity from tricyclic antidepressant (TCA) drugs
and other drugs that are sodium-channel blockers.
Sodium-channel blockade results in prolongation of
the QRS complex. If untreated, ventricular tachycar-
dia and ventricular fi brillation can ensue. If overdose
of these types of drugs is considered, it is important
to avoid class IA and IC antidysrhythmics, such as
amiodarone or procainamide.
49
Although sodium
bicarbonate is not routinely recommended in the
AHA guidelines for most cases of cardiac arrest, its
use is critically important in the setting of sodium-
channel toxicity. An overdose of either beta-blockers
or calcium-channel blockers also has dire clinical
consequences. Untreated overdose results in pulse-
less electrical activity or bradyasystolic cardiac
arrest. Intravenous bolus dosing of glucagon is used
in beta-blocker toxicity to assist with the regenera-
tion of metabolites necessary for effective cardiac
contraction; intravenous dosing of large quantities
of calcium is critical for reversal of calcium-channel
blockade in the setting of calcium-channel blocker
overdose.
CHAPTER 9
134
EKG evidence of STEMI, either before the cardiac
arrest or after resuscitation.
1–3
However, more recent
data show that early PCI may also improve the out-
comes for survivors of cardiac arrest without defi nite
evidence of STEMI on their EKG.
52,53
If further stud-
ies confi rm these fi ndings, it would strongly argue for
a signifi cant change in prehospital systems of care to
recommend that all survivors of cardiac arrest should
be immediately transported to hospitals that have the
capability to perform urgent PCI.
Out-of-hospital termination of resuscitation (TOR)
Finally, decades of research have established that sur-
vival rates for victims of cardiac arrest with nonshock-
able rhythms are extremely poor. Patients surviving
asystolic arrest are not likely to exhibit functional
neurologic recovery. Modern discussion of cardiac
arrest, therefore, incorporates the idea of termina-
tion of efforts. Rules for out-of-hospital termination
of resuscitation have shown reproducible results, and
several EMS systems already utilize preestablished
protocols for cessation of efforts.
54,55
Some of these so-
called “TOR rules” have been prospectively studied,
but are by no means without controversy. This strategy
acknowledges the high mortality associated with asys-
tolic arrest. Though the decision to stop resuscitation
is exceedingly complex, it makes little sense to refl ex-
ively mandate emergent transport for every victim of
prehospital cardiac arrest. There is general consensus
about which patients are unlikely to survive, and the
allocation of intensive care monitoring and personnel
to a clearly unsalvageable patient is impractical, costly,
and of questionable ethics. While each decision must
be made in the context of the individual patient and
family, it is part of the modern practice of Emergency
Medicine to not undertake futile expensive treatments.
This means increasing willingness to not extend futile
resuscitations, neither in the fi eld, nor in the ED.
Table 9-2 provides a sample TOR protocol.
56,57
Section IV: Decision making
Patients who suffer a witnessed cardiac arrest and •
have immediate bystander/EMS chest compressions
have the best chance at intact neurological survival.
Prehospital care must deliver early defi brillation, •
and avoid interruptions in compressions.
Discussion of cardiac arrest treatment cannot take
place without considering resource allocation. Victims
of cardiac arrest at all stages of their clinical course
demand meticulous attention to detail, signifi cant
expertise, and intensive monitoring. Those who sur-
vive the initial insult may depend upon a whole host of
support providers for their rehabilitation and recovery.
The costs associated with cardiac arrest are staggering.
Few patients survive neurologically intact; survivors
with hypoxic brain injury or encephalopathy often
require long-term, specialized nursing care.
13,14
Future directions in cardiac arrest care
Cardiocerebral resuscitation
The success of cardiocerebral resuscitation protocols
implemented in Arizona and Wisconsin prehospital
systems will likely result in modifi cations to advanced
cardiac life support treatment priorities.
12,14,17
Further
research into the optimal interplay of airway support
and circulatory support is ongoing, and if the results
of that research continue to support the principles of
cardiocerebral resuscitation, the traditional emergency
medicine focus on early airway support will be further
deemphasized for patients in cardiac arrest.
Urgent percutaneous intervention
Early coronary angiography and percutaneous cor-
onary intervention (PCI) is accepted as a valuable
treatment modality for patients who demonstrate
Table 9-1. Sample protocol for postarrest/therapeutic
hypothermia (TH) induction.
• Out of hospital:
• Begin external cooling for cardiac arrest survivors with
return of spontaneous circulation.
• Apply external cooling with ice packs to axillae and
groin and infusion of cold IV fl uids.
• Transport expeditiously to appropriate receiving facility.
• Emergency department
• Continue induction of TH for patients who remain
comatose.
• Monitor core temperature; cool to 32–34°C.
• Continue usual postresuscitation care (inotropic,
ventilator support as required).
• Critical Care Unit
• Maintain core temperature at 32–34°C for 24 hours.
• Consider invasive monitoring.