Full text of DOI:10.1080/10903120290938922

MANAGING THE POST-RESUSCITATION PATIENT IN THE FIELD
David E. Persse, MD, Brian S. Zachariah, MD, MBA, Jane G. Wigginton, MD
ABSTRACT
resuscitation. Unfortunately, to date,
no proven therapies are available to
improve neurologic outcome after
resuscitation from cardiac arrest. Key
words: cardiac arrest; post-resuscita-
tion syndrome; neurologic outcome;
resuscitation.
bances, oxygenation, ventilation,
acid–base balance, pulmonary
capacity, diffusion capabilities, car-
diac output, myocardial damage,
vascular conditioning, and blood
viscosity. For paramedics trying to
manage multiple physiologic
parameters in a relatively uncon-
trolled setting, the post-resuscita-
tion patient is one of their greatest
challenges. To facilitate success in
this endeavor, paramedics should
be provided guidelines for manag-
ing the post-resuscitation patient
that are easy to understand and
remember.
To produce useful guidelines for
post-resuscitation care, we must
identify the issues, review the cur-
rent understanding of the patho-
physiology unique to the resusci-
tated patient, discuss the current
state of the art regarding treatment
of resuscitated patients, and trans-
late this information into a product
that the average paramedic can
incorporate into care at the scene.
Among the areas that require spe-
cific attention in developing post-
resuscitation care guidelines are
post-resuscitation syndrome, man-
agement of post-resuscitation car-
diac dysfunction, and management
of post-resuscitation neurologic
dysfunction.
The principal goal after successful re-
suscitation of a cardiac arrest patient is
to maintain the patient’s pulse and
avoid a pulseless state. Of equal impor-
tance in the post-resuscitation patient
are efforts to prevent myocardial dys-
function and increase the likelihood of
a good neurologic outcome. To opti-
mize cardiac and hemodynamic resus-
citation, paramedics should obtain
good background information, which
could provide clues to factors con-
tributing to the cardiac arrest, such as
the use of certain drugs or being over-
due for dialysis, and could aid in cus-
tomizing therapy for rhythm distur-
bances and hemodynamic aberrations.
Treatment of rhythm disturbances
depends on the type of arrhythmia
identified, the history of present ill-
ness, and the resuscitation efforts pro-
vided. Common post-resuscitation
dysrhythmias are wide-complex tachy-
cardia, narrow-complex tachycardia,
and bradycardia. Optimizing neuro-
logic resuscitation is difficult, but evi-
dence suggests that hypertensive
reperfusion, hemodilution, and mild
hypothermia may be of benefit in
improving neurologic outcome after
PREHOSPITAL EMERGENCY CARE
2002;6:114–122
For the emergency medical servic-
es (EMS) provider, the immediate
goal of post-resuscitation manage-
ment is to maintain the patient’s
pulse, prevent recurrence of a
pulseless state, and optimize the
patient’s hemodynamic condition.
Once this has been achieved,
efforts should be made to achieve
the ultimate goal of post-resuscita-
tion management—enhancing the
likelihood that the patient will
have a good neurologic outcome.
Historically, the focus of EMS
and paramedic resuscitation train-
ing has been on reestablishing
spontaneous blood flow. The art of
stabilizing the critically ill survivor
of out-of-hospital cardiac arrest has
been given little emphasis, and
EMS personnel have received
almost no preparation on efforts to
ameliorate neurologic damage and
maximize a patient’s chance of
returning to a productive and
enjoyable life. This oversight is due
in part to the considerable efforts
made in training emergency med-
ical technicians and paramedics on
how to reestablish pulses and in
part to the relative lack of knowl-
edge regarding methods that can
be used in the early post-resuscita-
tion period that might increase the
likelihood of a good neurologic
outcome.
Received May 7, 2001, from the Department
of Emergency Medicine, University of
Texas–Houston
Medical
School,
Department of Surgery, Baylor College of
Medicine, and EMS, City of Houston (DEP),
Houston, Texas; Department of Emergency
Medicine, University of Louisville (BSZ),
Louisville, Kentucky; and Department of
Emergency Medicine, and EMS, University
of Texas Southwestern Medical Center
(JGW), Dallas, Texas. Revision received
August 17, 2001; accepted for publication
September 17, 2001.
POST-RESUSCITATION
SYNDROME
Negovsky1 first proposed the con-
cept of a specific post-resuscitation
disease in 1972. “Negovsky’s dis-
ease,” as it was known in early
work, was subsequently reclassi-
fied into a post-resuscitation syn-
drome consisting of four features:
1) reperfusion failure; 2) reoxy-
genation injury; 3) cerebral intoxi-
cation from derangement of extrac-
erebral organs; and 4) changes in
blood cell activity and coagulation
Presented at the Turtle Creek Conference
III, Dallas, Texas, April 29–May 1, 2001.
Supported by an unrestricted educational
grant from Wyeth-Ayerst Laboratories.
The hemodynamic stability of a
patient just resuscitated from car-
diac arrest is difficult to predict
and manage and depends on many
factors, including rhythm distur-
Address correspondence and reprint
requests to: David E. Persse, MD, Physician
Director of EMS, City of Houston, 601
Sawyer Street, Suite 500, Houston, TX 77007.
e-mail: <david.persse@cityofhouston.net>.
114

Persse et
alO.PST-RESUSCITATION CARE IN FIELD
115
abnormalities.2 Briefly, the overall
post-resuscitation syndrome is
believed to progress through sev-
eral stages, as outlined in Table 1.
The severity of the damage result-
ing from the ischemic insult that
initiates the post-resuscitation syn-
drome primarily depends on the
duration of anoxia (“no flow”) and
resuscitative efforts.
TABLE 1. Stages of Post-
resuscitation Syndrome
ATP. After blood flow and there-
fore oxygen delivery are restored,
hypoxanthine is oxidized with the
aid of xanthine oxidase, which
results in generation of oxygen-
derived free radicals, specifically
superoxide anions (O2–), hydroxy
radicals (–OH), and H2O2.16 These
active metabolites, collectively
referred to as oxygen-free radicals,
are believed to be responsible for
most reperfusion injury. Oxygen-
free radicals have been shown to
damage the sarcolemma and mito-
chondria,16,17 induce calcium over-
load in the cytoplasmic space,18,19
and produce cellular swelling,
lysosomal rupture, and myofibril-
lary contraction.20,21
Stage I (insult to 6 to 9 hours)
Rapid changes in cerebral and systemic
hemodynamics, clotting disturbances,
increased blood viscosity, multifocal tissue
hypoxia.
Stage II (10 to 24 hours)
Normalization of cardiovascular function,
persistent cerebral dysfunction, severely
impaired microcirculation. Fifty percent of
deaths occur during this period as a result
of recurrent cardiac arrest, bleeding, and
brain and lung edema.
Characteristics of Post-
resuscitation Myocardial
Dysfunction
Stage III (1 to 3 days)
Normalization of systemic indices,
improvement of cerebral function,
increased intestinal permeability leading to
bacteremia and development of multiple
organ dysfunction.
Transient coronary artery occlu-
sion results in temporary impair-
ment of myocardial capabilities.
This impairment will persist longer
and be more severe depending on
the duration of the ischemic
insult.3–7 The reversible ventricular
dysfunction phenomenon de-
scribed by Braunwald and Kloner8
has been labeled the “stunned
Stage IV (beyond 3 days)
Localized or generalized infection.
Characteristics of Post-
resuscitation Neurologic
Injury
sis, extracerebral organ derange-
ments, and blood derangements
due to stasis will lead to the struc-
tural incompetence of the neuron
and cellular death. Because these
processes are already under way
while the patient is being cared for
by the paramedic and before the
patient arrives at the hospital, there
may be little that can be done to
mitigate the damage caused by the
initial no-flow period. Efforts to
ameliorate neurologic dysfunction
in resuscitated patients using calci-
um channel blockers, anticonvul-
sants, free-radical scavengers, cor-
ticosteroids, and aminosteroids
have produced disappointing
results.24–27
A key characteristic of the post-
resuscitation syndrome is the loss
of cerebral autoregulation.28 In the
healthy brain, autoregulation
maintains a global cerebral blood
flow (gCBF) of about 50 mL per 100
g of brain tissue per minute within
the cerebral perfusion pressure
range of approximately 50 to 150
mm Hg. Cerebral perfusion pres-
sure is the mean arterial pressure
minus intracranial pressure. When
cerebral perfusion pressure drops
below 50 mm Hg, cerebral blood
flow decreases. The low-flow states
of cardiopulmonary resuscitation
The sudden no-flow state created
by cardiac arrest followed by the
low-flow state and incomplete
ischemia of cardiopulmonary re-
suscitation initiates the cerebral
ischemic insult that often results in
death or permanent disability.
Sudden and complete loss of cere-
bral perfusion followed by nor-
motensive reperfusion will pro-
duce the cerebral post-resuscita-
tion syndrome if the no-flow state
is of sufficient duration. This syn-
drome involves many complex
interactions of pathophysiologic
processes, including depletion of
ATP; respiratory (anaerobic) acido-
sis; failure of ATP-dependent ion
gradient maintenance efforts,
resulting in depolarization; calci-
um influx into the cell, resulting in
activation of calcium-dependent
enzymes, such as phospholipases
and proteases, that degrade cell
membranes and certain proteins;
and glutamate release, resulting in
excitotoxicity of neurons.22,23
myocardium.”
Although
the
stunned myocardium dysfunction
and recovery phenomenon was
first described in terms of regional
ischemia, it has also been observed
in the setting of cardiac arrest and
resuscitation.9–11
The exact mechanisms believed
to be responsible for myocardial
dysfunction after global ischemia
remain unclear. However, the fol-
lowing theories are the two most
generally accepted:
Depletion of high-energy phosphates
theory. This theory is based on the
observation that myocardial mito-
chondria depend heavily on oxy-
gen and aerobic metabolism to pro-
duce adenosine triphosphate
(ATP). In dogs, mitochondrial
recovery from global ischemia can
take as long as 72 hours despite
adequate reperfusion.12–15
Reperfusion injury theory. This
theory suggests that there is little
damage to the myocyte during the
no-flow period and that the dam-
age actually occurs when circula-
tion is restored. Aerobic oxidative
phosphorylation is reduced and
hypoxanthine accumulates as a
consequence of degradation of
After reperfusion, brain ATP, ion
pumps, and tissue pH quickly
return to normal. However, perfu-
sion failure, reoxygenation injury
with chemical cascades leading to
lipid peroxidation and cell necro-

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PREHOSPITAL EMERGENCY CARE JANUARY / MARCH 2002 VOLUME 6 / NUMBER 1
threaten the viability of normal
neurons, with cerebral perfusion
pressures of less than 30 mm Hg
allowing for cerebral blood flow of
less than 15 mL per 100 g of brain
tissue per minute. Inadequate oxy-
gen delivery is evidenced by a
cerebral venous oxygen tension of
less than 20 torr.28–30 The brain may
tolerate low flow (gCBF of 10% of
normal) better than no flow,31 but
“trickle flow” (gCBF < 10%) can
sometimes be worse than no
flow.32
low gCBF and cerebral oxygen
consumption, which is a clini-
cal indicator of brain death.
and should not be treated. Other
medications will have more pro-
longed effects on the heart, blood
vessels, and other organs and may
contribute substantially to the diffi-
culties encountered trying to stabi-
lize a patient.
Common post-resuscitation dys-
rhythmias can be categorized as
wide-complex tachycardia, nar-
row-complex tachycardia, and
bradycardia, which is often associ-
ated with varying degrees of atri-
oventricular block.
OPTIMIZING CARDIAC
AND HEMODYNAMIC
RESUSCITATION
Immediately after restoring the
patient’s pulse, paramedics typi-
cally focus on the continued pres-
ence of a pulse and the patient’s
rhythm. Because the scene of a car-
diac arrest resuscitation is often
chaotic, it can be difficult for para-
medics to obtain background infor-
mation. Nonetheless, they should
try to determine whether a resusci-
tated patient’s rhythm disturbance
is intrinsic to the cause of the car-
diac arrest or a result of the resus-
citative efforts. The contribution of
tricyclic antidepressants, beta-
blockers, calcium channel blockers,
cocaine, amphetamines, pesticides,
missed dialysis, history of accesso-
ry pathways, and other conditions
may not be appreciated unless
EMS providers specifically ask
about these conditions. Often hints
to these contributors are present in
the prodromal symptoms the
patient reported before collapse or
the physical signs noticed either
before collapse or during the early
stages of resuscitation. Conversely,
rescuers should remember that in
many patients with classic sudden
death syndrome, the heart has no
structural or vascular abnormali-
ties.
Resuscitation medications are a
common extrinsic cause of rhythm
disturbances in the post-resuscita-
tion patient. Epinephrine is a
potent cause of tachydysrhythmia.
Atropine also can contribute to the
development of tachycardias.
Lidocaine, amiodarone, and other
antiarrhythmics can contribute to
arrhythmia problems as well.
Epinephrine and lidocaine have
short half-lives and will be quickly
metabolized. Thus their effects,
such as tachycardia and profound
hypertension from epinephrine,
will dissipate over several minutes
Cerebral blood-flow problems
(i.e., reperfusion failure) in the
post-resuscitation patient progress
through four stages:
Wide-complex Tachycardia
In non-cardiac-arrest settings, dif-
ferentiating ventricular tachycar-
dia (VT) from a supraventricular
rhythm with aberrant conduction
may be difficult, but wide-complex
tachycardia is most often VT.
However, in the immediate post-
resuscitation patient with a pulse,
this is quite likely not the case. A
heart that has been subjected to
global ischemia and then develops
VT is not likely to sustain a pulsing
VT for long and can be expected to
deteriorate into ventricular fibrilla-
tion quickly. Therefore, if a just-
resuscitated patient with a pulse
has a wide-complex tachycardia,
the patient likely has a supraven-
tricular rhythm with aberrant con-
duction. Treatment of this rhythm
with synchronized countershock or
antiarrhythmics may be unneces-
sary and quite possibly detrimental
to the patient.
1. Multifocal no reflow occurs
immediately and seems to be
readily overcome by nor-
motensive or hypertensive
reperfusion.33,34 After pulses
are restored, patients demon-
strate a post-arrest no-reflow
phenomenon that can be over-
come when reperfusion pres-
sure is high.33,35
2. Transient global “reactive” hyper-
emia (vasoparalysis) lasts 10 to
30 minutes.33,36–38 The hyper-
emic flow patterns are believed
to last longer in the brain stem
and basal ganglia than in the
neocortex.
3. Delayed, prolonged, global and
multifocal hypoperfusion begins
about two hours after circula-
tion is restored. After the tran-
sient period of hyperemia,
gCBF is decreased to as little as
50% of normal because of loss
of autoregulation capabili-
ties.33,36,38–40 Despite the hyper-
perfusion continuing in some
limited areas of the brain, gCBF
is reduced to about 50% of
baseline, while cerebral meta-
bolic oxygen consumption re-
turns to or above baseline val-
ues, creating a mismatch of
oxygen delivery and up-
take.33,36–38,41
Narrow-complex
Tachycardia
In patients with narrow-complex
tachycardia after resuscitation, the
indicated therapy is often conser-
vative “watchful waiting,” particu-
larly if the patient has received
intravenous epinephrine. The
International Resuscitation Guide-
lines 2000 recommend counter-
shock for narrow-complex tachy-
cardia of more than 150 beats/min
only when the patient has serious
signs and symptoms related to the
tachycardia (e.g., chest pain, short-
4. Late resolution is marked by
either normal gCBF and cere-
bral oxygen consumption or

Persse et
alO.PST-RESUSCITATION CARE IN FIELD
117
TABLE 2. Methods of Optimizing
Neurologic Resuscitation
ness of breath, decreased level of
consciousness, low blood pressure,
shock, pulmonary congestion, con-
gestive heart failure, or acute
myocardial infarction).42 In the
post-arrest setting, the signs and
symptoms of critical illness (e.g.,
unresponsiveness, hypotension)
are likely to be related to the anox-
ic or hypoxic period, and the tachy-
cardia is either protective or simply
the effect of epinephrine. There-
fore, the tachycardia should not
necessarily be treated as if it were a
presenting sign. Patients with rap-
idly progressive tachycardia dete-
riorating into ventricular fibrilla-
tion may be demonstrating the
effects of administered epineph-
rine. As a result, a conservative
approach to the post-resuscitation
patient with tachycardia that
allows the beta-adrenergic effects
of epinephrine to subside may
enhance the likelihood of the
patient’s developing a normal rate
and pressure.
regarding cerebral dysfunction
after cardiopulmonary arrest is
that pathophysiologic processes
are initially set into motion during
the hyperemic period after restora-
tion of normotensive reperfusion.
Increasing evidence indicates that
continued neurologic damage
occurs by further initiation of the
same and other pathophysiologic
processes during the nonhomoge-
neous flow patterns that develop
shortly after return of spontaneous
circulation.22,23 Therefore, efforts to
minimize or eliminate the nonho-
mogeneous flow patterns of the
post-resuscitation patient should
be helpful. Among them are hyper-
tensive reperfusion, hemodilution,
and mild hypothermia (Table 2).
Hypertensive reperfusion
Aim for a systolic blood pressure that is
higher than normal (i.e., 150 mm Hg).
Hemodilution
Promote increased cerebral blood flow by
providing hemodilution (normal saline) as
part of the vasopressor support.
Mild hypothermia
Allow for mild hypothermia to begin by
stripping the patient to undergarments and
avoiding anything that would increase the
patient’s body temperature.
els, hypertensive reperfusion can
overcome the immediate no-reflow
phenomenon,33,34,38 enhance circu-
lation to the vulnerable brain areas,
and improve electroencephalo-
graphic recovery.47 In a dog model
of cardiac arrest, a brief episode of
induced hypertension (mean arte-
rial pressure of 150 to 200 mm Hg
for 1 to 5 minutes) followed by con-
trolled normotension eliminated
evidence of immediate cerebral no
reflow and correlated with improv-
ed cerebral outcome.35 After return
of spontaneous circulation in
humans, brief hypertension corre-
lates with a good cerebral outcome
and hypotension with a poor cere-
bral outcome.48,49 However, pro-
longed severe hypertension after
cardiac arrest might not be tolerat-
ed by the ischemic heart and can
worsen vasogenic cerebral ede-
ma.43,50
Hypertensive Reperfusion
Soon after spontaneous circulation
is restored, a fairly short-lived
increase in cerebral blood flow
occurs. This hyperemic period lasts
from 10 to 30 minutes. The hyper-
emic flow patterns are believed to
last longer in the brain stem and
basal ganglia than in the neocortex.
Following the hyperemic period is
a period of variable perfusion to
vulnerable regions of the brain.
Multiple studies have demonstrat-
ed cellular morphologic changes in
these brain areas that are believed
to represent post-ischemic brain
damage.35,43–45 This damage is
believed to result from mismatch
of cerebral oxygen consumption
and delivery.
As previously mentioned, a seri-
ous sequela of cerebral ischemia is
the loss of autoregulation of cere-
bral blood flow.28 Evidence sug-
gests that induced hypertension or
enhanced flow states might over-
come problems resulting from loss
of autoregulation.33,35,46 During the
period of decreased cerebral blood
flow, vulnerable regions in the
brain are usually more severely
damaged. These areas are charac-
teristically found in the border
zones between cerebral arterial dis-
tribution zones.22,23 In animal mod-
Bradycardia
Most patients resuscitated from
cardiac arrest who are bradycardic
are suffering from either serious
conduction abnormalities or global
myocardial ischemia. Treatment
options are to pace the heart,
administer atropine, or do nothing.
In a hypotensive post-resuscitation
patient with a bradycardic rhythm,
atropine can generally be given
quickly in most EMS systems.
However, for those systems
equipped with transthoracic pac-
ing capabilities, pacing is the inter-
vention of choice.
Hemodilution
A contributing factor to the no-
reflow phenomenon is sludging.
Consequently, hemodilution has
been shown to be effective in
increasing cerebral blood flow.33,35
Post-ischemic hypoperfusion can
be prevented by hypertensive
reperfusion plus normovolemic
hemodilution.33 However, hemodi-
lution is not without its dangers.
Overdilution to hematocrit values
of less than 30% can decrease arte-
rial oxygen transport capabilities
even with increased cardiac output
and cerebral blood flow. A hemat-
ocrit of 30% seems beneficial.45
OPTIMIZING NEUROLOGIC
RESUSCITATION
Currently, beyond providing high-
flow oxygen and striving to main-
tain a heart beat, EMS providers do
little specifically to resuscitate the
brain. Current research suggests
there may be some things para-
medics can do to improve the neu-
rologic outcome of cardiac arrest
survivors. An emerging theory

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PREHOSPITAL EMERGENCY CARE JANUARY / MARCH 2002 VOLUME 6 / NUMBER 1
bined with mild hypothermia have
Mild Hypothermia
CONCLUSION
been remarkably successful.70,71
Deep hypothermia (<25°C) causes
ventricular fibrillation or asystole
but is successfully used in the oper-
ative theater. Moderate hypother-
mia (30°C), induced before circula-
tory arrest, protects the brain dur-
ing no flow of up to 20 minutes.
Mild hypothermia (33–34°C) can
improve neurologic outcomes in
select patients with stroke or head
trauma.51–55 Mild hypothermia has
also shown promise in multiple
cardiac arrest studies in ani-
mals.44,56–61 This benefit, however,
seems highly time-dependent, with
improved outcomes seen only
when mild hypothermia is initiat-
ed and achieved early in the post-
resuscitation period.62,63 The use of
mild hypothermia in human sur-
vivors of cardiac arrest has shown
promise and is believed to be
safe.64–69
Resuscitating a patient who has
suffered cardiac arrest is a consid-
erable accomplishment, but to
achieve the best possible patient
outcome, post-resuscitation myo-
cardial dysfunction and neurologic
injury must be minimized. To do
so, paramedics must recognize the
various types of arrhythmias that
can occur after resuscitation and
take appropriate steps to end the
abnormal rhythm. Arrhythmias in
the resuscitated patient can be due
to a variety of etiologies different
from those in the non-arrested
patient, and the patient must be
treated accordingly. Neurologic
injury resulting from decreased
cerebral blood flow can be difficult
to prevent or minimize, but use of
hypertensive reperfusion, hemodi-
lution, and mild hypothermia has
shown promise in improving neu-
rologic outcomes. Furthermore,
maintenance of normal PaCO2 lev-
els measured by capnometry will
decrease the likelihood of iatro-
genic inhibition of cerebral blood
flow.
Hyperventilation
Overaggressive hyperventilation
can impair cerebral blood flow and
promote cerebral edema in post-
resuscitation patients.72 Historical-
ly, hyperventilation has been rec-
ommended to reverse the metabol-
ic acidosis that has accumulated
during the cardiac arrest. Problems
with hyperventilation are now rec-
ognized, specifically in terms of
reduced cerebral blood flow result-
ing from hypocarbic vasoconstric-
tion. During the period of cerebral
oxygen debt, a decrease in oxygen
delivery resulting from reduced
blood flow must be avoided.
Capnography and capnometry
devices are available to EMS per-
sonnel and can reliably guide para-
medics as to the arterial carbon
dioxide content. While the patient
has evidence of adequate cardiac
output (i.e., easily palpable pulses),
the patient’s ventilations should be
titrated to maintain end-tidal car-
bon dioxide levels near 40 mm Hg
or just below.
A variety of animal studies look-
ing at single interventions has pro-
duced disappointing results com-
pared with some using combina-
tion therapy. Animal studies using
a combination of techniques to
improve cerebral blood flow com-

Persse et
alO.PST-RESUSCITATION CARE IN FIELD
119
CONSENSUS PRESENTATION
pants agreed that not enough data
were available to support such a
recommendation.
line therapy. Although no strong
evidence indicates that pacing is
any more effective than atropine in
a bradycardic patient, it can be
done fairly quickly, particularly if
combination pads have been used
for the cardiac arrest, and its effects
are quickly reversible, simply by
shutting off the machine. Atropine,
which can also be administered
fairly quickly, cannot be “turned
off” as can pacing if adverse effects
develop. Little evidence supports
the use of a vasopressor in post-
resuscitation bradycardia.
The consensus group did agree
that bradycardia in the post-resus-
citation patient should be treated
more aggressively than it currently
is. Paramedics are traditionally
taught that bradycardia in a patient
who is not hypotensive is of little
concern. This philosophy may be
changing, as more data accumulate
on the potential benefits of a high-
er-than-normal blood pressure in
bradycardic post-resuscitation pa-
tients.
“I’ve got a pulse back; what do I
do now?” This was the overriding
question the consensus group
sought to answer, as they ad-
dressed several aspects of post-
resuscitation care of the adult car-
diac arrest patient. The consensus
participants agreed that after a
patient is successfully resuscitated,
the goal is to maintain hemody-
namic stability through appropri-
ate management of arrhythmias
and blood pressure and to improve
neurologic outcome.
The second step in managing the
hypotensive tachycardic patient
after resuscitation is to administer
fluids, unless there is clear evi-
dence of volume overload. The rec-
ommendation was to start with 250
to 500 mL of normal saline, to
repeat this dose if the patient
remained hypotensive, and to
titrate the dose to effect or adverse
effects. Although most textbooks
recommend starting with fluids
and then adding either an inotrope
or a vasopressor, the consensus
group did not endorse this
approach, given the paucity of data
in this area. The primary concern
of the consensus participants was
that it is difficult to determine in
the field whether a patient has a
significant left ventricular wall
abnormality or impaired systemic
vascular resistance. It is also often
difficult to determine whether the
patient is hypotensive secondary to
a tachycardia or tachycardic sec-
ondary to hypotension. Accurately
identifying the underlying prob-
lem based on history or physical
examination might not be possible.
Thus empirically adding either an
inotrope or a vasopressor might
not only be ineffective but could
even be harmful to the patient. The
best approach for these patients is
to administer fluids, monitor for
signs of pulmonary edema, and
rapidly transport them to the hos-
pital. However, during transport,
RHYTHM DISTURBANCES
Post-resuscitation rhythm distur-
bances can be categorized as either
tachycardias (wide complex or nar-
row complex) or bradycardia and
as either intrinsically abnormal or
extrinsically abnormal (i.e., result-
ing from the effects of the resusci-
tation attempt itself). Most tachy-
cardias that occur after resuscita-
tion are likely due to the cate-
cholamine release that accompa-
nies the arrest or the treatment of
the arrest itself. Unless the patient
is hypotensive, “watchful waiting”
is the recommended approach for
post-resuscitation tachycardias.
For the hypotensive patient who
becomes tachycardic after resusci-
tation, the first step is to determine
whether the rhythm disturbance is
sinus tachycardia or some other
tachyarrhythmia. A 12-lead elec-
trocardiogram is useful in making
this distinction and in determining
whether an acute myocardial
infarction was the cause of the car-
diac arrest. Patients who suffer
arrest secondary to an acute
myocardial infarction or other
treatable etiology can potentially
benefit from being transported to a
facility equipped with a catheteri-
zation laboratory. The group con-
sidered whether all post-resuscita-
tion patients should be transported
to such a facility, but the partici-
BLOOD PRESSURE
Patients who are hypertensive after
resuscitation from cardiac arrest
tend to have better outcomes than
do those who are hypotensive.
Whether hypertension is a marker
for patients who will do better or
whether the hypertension itself con-
tributes to better outcomes is
unclear. In any case, given the
potential benefits of hypertension,
post-resuscitation patients who are
hypotensive should not be given
high-dose dopamine as a single
agent unless vasodilation is clearly
the cause of the hypotension. The
difficulty in differentiating primary
paramedics
should
continue
aggressive ventilatory manage-
ment and constant reassessment.
Bradycardia in the post-resusci-
tation patient is primarily due to
ventilatory problems, such as poor
airway management or poor venti-
lation. The first task, then, is to look
for potential causes of impaired
ventilation. Pacing the bradycardic
heart is generally considered first-
tachycardia
with
secondary
hypotension from primary hypo-
tension with secondary tachycardia
was
previously
mentioned.
Acknowledging that concern, the
consensus group noted that com-
bining dopamine with norepineph-

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PREHOSPITAL EMERGENCY CARE JANUARY / MARCH 2002 VOLUME 6 / NUMBER 1
rine may be of benefit in hypoten-
sive post-arrest patients, because
these patients often are relatively
volume-depleted and vasodilated.
However, most data supporting use
of this combination were gathered
from septic shock models rather
than true post-resuscitation cardiac
arrest models. Dobutamine might
also be a good choice for post-resus-
citation hypotension. However,
until further data are available, the
consensus group would not make
any strong recommendation on the
management of post-resuscitation
hypotension beyond the adminis-
tration of fluids.
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The consensus participants agreed
that gathering useful data in the
field on post-resuscitation care is
difficult. The group did recom-
mend use of end-tidal carbon diox-
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and monitor endotracheal tube
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CONCLUSION
Few data are available on post-
resuscitation care of the cardiac
arrest patient. What data are avail-
able have come mostly from other
models, such as those for septic
shock. Nonetheless, paramedics
can take steps to improve the out-
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including appropriate manage-
ment of arrhythmias, blood pres-
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future, improved modalities for
cardiopulmonary resuscitation and
minimally invasive thoracotomy
procedures may lead not only to
improved resuscitation but also to
improved cerebral perfusion pres-
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Although the consensus partici-
pants had several recommenda-
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they emphasized that rapid return
of spontaneous circulation is the
cornerstone of good post-resuscita-
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medical services providers should
not become so focused on treating
complications or drug adverse
effects that they ignore the fact that
the best means of avoiding neuro-
logic injury is to achieve return of
spontaneous circulation as quickly
as possible.
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an appropriate temperature might
be possible in the future. At pres-
ent, the consensus group recom-
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patient’s clothing to the limits of
the environment. Patients can then
cool passively but should not be
allowed to become overly hypo-
thermic (<30°C).
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treated aggressively.
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