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DOI: 10.1161/CIRCULATIONAHA.105.166560
2005;112;84-88; originally published online Nov 28, 2005; Circulation
Part 7.5: Postresuscitation Support
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Part 7.5: Postresuscitation Support
F
ew randomized controlled clinical trials deal specifically
with supportive care following cardio-pulmonary-
cerebral resuscitation (CPCR) from cardiac arrest. Neverthe-
less, postresuscitation care has significant potential to im-
prove early mortality caused by hemodynamic instability and
multi-organ failure and later mortality/morbidity resulting
from brain injury.
1
This section summarizes our evolving
understanding of the hemodynamic, neurologic, and metabol-
ic abnormalities encountered in patients who are resuscitated
from cardiac arrest.
Initial objectives of postresuscitation care are to
●
Optimize cardiopulmonary function and systemic perfu-
sion, especially perfusion to the brain
●
Transport the victim of out-of-hospital cardiac arrest to the
hospital emergency department (ED) and continue care in
an appropriately equipped critical care unit
●
Try to identify the precipitating causes of the arrest
●
Institute measures to prevent recurrence
●
Institute measures that may improve long-term, neurolog-
ically intact survival
Improving Postresuscitation Outcomes
Postresuscitation care is a critical component of advanced life
support. Patient mortality remains high after return of spon-
taneous circulation (ROSC) and initial stabilization. Ultimate
prognosis in the first 72 hours may be difficult to determine,
2
yet survivors of cardiac arrest have the potential to lead
normal lives.
3–5
During postresuscitation care providers
should (1) optimize hemodynamic, respiratory, and neuro-
logic support; (2) identify and treat reversible causes of
arrest; and (3) monitor temperature and consider treatment for
disturbances of temperature regulation and metabolism. The
first sections below discuss initial stabilization and tempera-
ture/metabolic factors that may be relevant to improving
postresuscitation outcome, particularly in the critically ill
survivor. Subsequent sections highlight organ-specific eval-
uation and support.
Return of Spontaneous Circulation
The principal objective of postresuscitation care is the re-
establishment of effective perfusion of organs and tissue.
After ROSC in the out-of-hospital or in-hospital setting, the
provider must consider and treat the cause of the arrest and
the consequences of any hypoxemic/ischemic/reperfusion
injury. In most cases the acidemia associated with cardiac
arrest improves spontaneously when adequate ventilation and
perfusion are restored. But restoration of blood pressure and
improvement in gas exchange do not ensure survival and
functional recovery. Significant myocardial stunning and
hemodynamic instability can develop, requiring vasopressor
support. Most postresuscitation deaths occur during the first
24 hours.
6,7
Ideally the patient will be awake, responsive, and breathing
spontaneously. Alternatively the patient may initially be
comatose but have the potential for full recovery after
postresuscitation care.
3
Indeed, up to 20% of initially coma-
tose survivors of cardiac arrest have been reported to have
good 1-year neurologic outcome.
8
The pathway to the best
hospital postresuscitation care of all initial survivors is not
completely known, but there is increasing interest in identi-
fying and optimizing practices that can improve outcome.
9
Regardless of the patient’s initial status, the provider should
support adequate airway and breathing, administer supple-
mentary oxygen, monitor the patient’s vital signs, establish or
verify existing intravenous access, and verify the function of
any catheters in place.
The clinician should assess the patient frequently and treat
abnormalities of vital signs or cardiac arrhythmias and
request studies that will further aid in the evaluation of the
patient. It is important to identify and treat any cardiac,
electrolyte, toxicologic, pulmonary, and neurologic precipi-
tants of arrest. The clinician may find it helpful to review the
H’s and T’s mnemonic to recall factors that may contribute to
cardiac arrest or complicate resuscitation or postresuscitation
care: hypovolemia, hypoxia, hydrogen ion (acidosis), hyper-/
hypokalemia, hypoglycemia, hypothermia; toxins, tamponade
(cardiac), tension pneumothorax, thrombosis of the coronary
or pulmonary vasculature, and trauma. For further informa-
tion see Part 10: “Special Resuscitation Situations.”
After initial assessment and stabilization of airway, venti-
lation, and circulation, transfer the patient to a special care
unit for observation, continuous monitoring, and further
therapy. Personnel with appropriate training and resuscitation
equipment must accompany the patient during transport to the
special care unit.
Temperature Regulation
Induced Hypothermia
Both permissive hypothermia (allowing a mild degree of
hypothermia H1102233°C [91.5°F] that often develops spontane-
ously after arrest) and active induction of hypothermia may
play a role in postresuscitation care. In 2 randomized clinical
trials (LOE 1
3
; LOE 2
4
) induced hypothermia (cooling within
minutes to hours after ROSC) resulted in improved outcome
in adults who remained comatose after initial resuscitation
from out-of-hospital ventricular fibrillation (VF) cardiac ar-
rest. Patients in the study were cooled to 33°C (91.5°F)
3
or to
the range of 32°C to 34°C (89.6°F to 93.2°F)
4
for 12 to 24
hours. The Hypothermia After Cardiac Arrest (HACA) study
3
included a small subset of patients with in-hospital cardiac
arrest.
(Circulation. 2005;000:IV-84-IV-88.)
? 2005 American Heart Association.
This special supplement to Circulation is freely available at
http://www.circulationaha.org
DOI: 10.1161/CIRCULATIONAHA.105.166560
IV-84
A third study (LOE 2)
10
documented improvement in
metabolic end points (lactate and O
2
extraction) when coma-
tose adult patients were cooled after ROSC from out-of-
hospital cardiac arrest in which the initial rhythm was
pulseless electrical activity (PEA)/asystole.
In the HACA
3
and Bernard
4
studies, only about 8% of
patients with cardiac arrest were selected for induced hypo-
thermia (ie, patients were hemodynamically stable but coma-
tose after a witnessed arrest of presumed cardiac etiology).
This highlights the importance of identifying the subset of
patients who may most benefit. Although the number of
patients who may benefit from hypothermia induction is
limited at present, it is possible that with more rapid and
controlled cooling and better insights into optimal target
temperature, timing, duration, and mechanism of action, such
cooling may prove more widely beneficial in the future.
11
A
recent multicenter study in asphyxiated neonates showed that
hypothermia can be beneficial in another select population.
12
Complications associated with cooling can include coagu-
lopathy and arrhythmias, particularly with an unintentional
drop below target temperature. Although not significantly
higher, cases of pneumonia and sepsis increased in the
hypothermia-induction group.
3,4
Cooling may also increase
hyperglycemia.
4
Most clinical studies of cooling have used external cooling
techniques (eg, cooling blankets and frequent applications of
ice bags) that may require a number of hours to attain target
temperature. More recent studies
13
suggest that internal cool-
ing techniques (eg, cold saline, endovascular cooling cathe-
ter) can also be used to induce hypothermia. Providers should
continuously monitor the patient’s temperature during
cooling.
3,4
In summary, providers should not actively rewarm hemo-
dynamically stable patients who spontaneously develop a
mild degree of hypothermia (H1102233°C [91.5°F]) after resusci-
tation from cardiac arrest. Mild hypothermia may be benefi-
cial to neurologic outcome and is likely to be well tolerated
without significant risk of complications. In a select subset of
patients who were initially comatose but hemodynamically
stable after a witnessed VF arrest of presumed cardiac
etiology, active induction of hypothermia was beneficial.
3,4,13
Thus, unconscious adult patients with ROSC after out-of-
hospital cardiac arrest should be cooled to 32°C to 34°C
(89.6°F to 93.2°F) for 12 to 24 hours when the initial rhythm
was VF (Class IIa). Similar therapy may be beneficial for
patients with non-VF arrest out of hospital or for in-hospital
arrest (Class IIb).
Hyperthermia
After resuscitation, temperature elevation above normal can
create a significant imbalance between oxygen supply and
demand that can impair brain recovery. Few studies (with
either frequent use of antipyretics or “controlled normother-
mia” with cooling techniques) have directly examined the
effect of temperature control immediately after resuscitation.
Because fever may be a symptom of brain injury, it may be
difficult to control it with conventional antipyretics. Many
studies of brain injury in animal models, however, show
exacerbation of injury if body/brain temperature is increased
during or after resuscitation from cardiac arrest.
14–17
More-
over, several studies have documented worse neurologic
outcome in humans with fever after cardiac arrest (LOE 3)
18
and ischemic brain injury (LOE 7 extrapolated from stroke
victims
18
). Thus, the provider should monitor the patient’s
temperature after resuscitation and avoid hyperthermia.
Glucose Control
The postresuscitation patient is likely to develop electrolyte
abnormalities that may be detrimental to recovery. Although
many studies have documented a strong association between
high blood glucose after resuscitation from cardiac arrest and
poor neurologic outcomes (LOE 4
21,22
; LOE 5
9,22–26
; LOE
6
27
), they did not show that control of serum glucose level
alters outcome.
A prospective randomized study by van den Berghe (LOE
1)
28
did show that tight control of blood glucose using insulin
reduced hospital mortality rates in critically ill patients who
required mechanical ventilation. The study did not specifi-
cally focus on postresuscitation patients, but the effect of
blood glucose control on outcome is compelling. The study
documented not only improved survival but decreased mor-
tality from infectious complications, a common problem in
the postresuscitation setting.
In comatose patients, signs of hypoglycemia are less
apparent, so clinicians must monitor serum glucose closely to
avoid hypoglycemia when treating hyperglycemia. On the
basis of findings of improved outcomes in critically ill
patients when glucose levels are maintained in the normal
range, it is reasonable for providers to maintain strict glucose
control during the postresuscitation period. Additional study
is needed, however, to identify the precise blood glucose
concentration that requires insulin therapy, the target range of
blood glucose concentration, and the effect of tight glucose
control on outcomes of patients after cardiac arrest.
Organ-Specific Evaluation and Support
After ROSC patients may remain comatose or have decreased
responsiveness for a variable period of time. If spontaneous
breathing is absent or inadequate, mechanical ventilation via
an endotracheal tube or other advanced airway device may be
required. Hemodynamic status may be unstable with abnor-
malities of cardiac rate, rhythm, systemic blood pressure, and
organ perfusion.
Clinicians must prevent, detect, and treat hypoxemia and
hypotension because these conditions can exacerbate brain
injury. Clinicians should determine the baseline postarrest
status of each organ system and support organ function as
needed.
The remainder of this chapter focuses on organ-specific
measures that should be provided in the immediate postresus-
citation period.
Respiratory System
After ROSC patients may exhibit respiratory dysfunction.
Some patients will remain dependent on mechanical ventila-
tion and will need an increased inspired concentration of
oxygen. Providers should perform a full physical examination
and evaluate the chest radiograph to verify appropriate
Part 7.5: Postresuscitation Support IV-85
endotracheal tube depth of insertion and identify cardiopul-
monary complications of resuscitation. Providers should ad-
just mechanical ventilatory support based on the patient’s
blood gas values, respiratory rate, and work of breathing. As
the patient’s spontaneous ventilation becomes more efficient,
the level of respiratory support may be decreased until
spontaneous respiration returns. If the patient continues to
require high inspired oxygen concentrations, providers should
determine if the cause is pulmonary or cardiac and direct care
accordingly.
Debate exists as to the length of time patients who require
ventilatory support should remain sedated. To date there is
little evidence to guide therapy. One observational study
(LOE 3)
29
found an association between use of sedation and
development of pneumonia in intubated patients during the
first 48 hours of therapy. The study, however, was not
designed to investigate sedation as a risk factor for either
pneumonia or death in patients with cardiac arrest. At this
time there is inadequate data to recommend for or against the
use of a defined period of sedation or neuromuscular block-
ade after cardiac arrest (Class Indeterminate). Use of neuro-
muscular blocking agents should be kept to a minimum
because these agents preclude thorough neurologic assess-
ments during the first 12 to 72 hours after ROSC.
2
Sedation may be necessary to control shivering during
hypothermia. If shivering continues despite optimal sedation,
neuromuscular blockade may be required in addition to deep
sedation.
Ventilatory Parameters
Sustained hypocapnea (low PCO
2
) may reduce cerebral blood
flow.
30–31
After cardiac arrest, restoration of blood flow
results in an initial hyperemic blood flow response that lasts
10 to 30 minutes, followed by a more prolonged period of low
blood flow.
32,33
During this latter period of late hypoperfu-
sion, a mismatch between blood flow (oxygen delivery) and
oxygen requirement may occur. If the patient is hyperventi-
lated at this stage, cerebral vasoconstriction may further
decrease cerebral blood flow and increase cerebral ischemia
and ischemic injury.
There is no evidence that hyperventilation protects the
brain or other vital organs from further ischemic damage after
cardiac arrest. In fact, Safar et al
34
provided evidence that
hyperventilation may worsen neurologic outcome. Hyperven-
tilation may also generate increased airway pressures and
augment intrinsic positive end-expiratory pressure (so-called
“auto PEEP”), leading to an increase in cerebral venous and
intracranial pressures.
35,36
Increases in cerebral venous pres-
sure can decrease cerebral blood flow and increase brain
ischemia.
In summary, no data supports targeting a specific arterial
PaCO
2
level after resuscitation from cardiac arrest. But data
extrapolated from patients with brain injury supports venti-
lation to normocarbic levels as appropriate. Routine hyper-
ventilation is detrimental (Class III).
Cardiovascular System
Both the ischemia/reperfusion of cardiac arrest and electrical
defibrillation can cause transient myocardial stunning and
dysfunction
37
that can last many hours but may improve with
vasopressors.
38
Cardiac biomarker levels may be increased in
association with global ischemia caused by absent or de-
creased coronary blood flow during cardiac arrest and CPR.
Increased cardiac biomarkers may also indicate acute myo-
cardial infarction as the cause of cardiac arrest.
Hemodynamic instability is common after cardiac arrest,
and early death due to multi-organ failure is associated with
a persistently low cardiac index during the first 24 hours after
resuscitation (LOE 5).
6,39
Thus, after resuscitation clinicians
should evaluate the patient’s electrocardiogram, radiographs,
and laboratory analyses of serum electrolytes and cardiac
biomarkers. Echocardiographic evaluation within the first 24
hours after arrest is useful to guide ongoing management.
5,40
One large case series (LOE 5)
6
of patients resuscitated
following out-of-hospital cardiac arrest documented signifi-
cant early but reversible myocardial dysfunction and low
cardiac output, followed by later vasodilation. The hemody-
namic instability responded to fluid administration and vaso-
active support.
6
Invasive monitoring may be necessary to
measure blood pressure accurately and to determine the most
appropriate combination of medications to optimize blood
flow and distribution. The provider should titrate volume
administration and vasoactive (eg, norepinephrine), inotropic
(eg, dobutamine), and inodilator (eg, milrinone) drugs as
needed to support blood pressure, cardiac index, and systemic
perfusion. The ideal target blood pressure or hemodynamic
parameters associated with optimal survival have not been
established.
Both cardiac arrest and sepsis are thought to involve
multi-organ ischemic injury and microcirculatory dysfunc-
tion. Goal-directed therapy with volume and vasoactive drug
administration has been effective in improving survival from
sepsis.
41
The greatest survival benefit is due to a decreased
incidence of acute hemodynamic collapse, a challenge also
seen in the postresuscitation setting. Data extrapolated from a
study of goal-directed therapy for sepsis (LOE 1
41
for sepsis;
LOE 7 [extrapolated] for cardiac arrest) suggests that provid-
ers should try to normalize oxygen content and oxygen
transport.
Relative adrenal insufficiency may develop following the
stress of cardiac arrest, but the use of early corticosteroid
supplementation in such patients to improve either hemody-
namics or outcome is unproven and requires further
evaluation.
42
Although sudden cardiac arrest may be precipitated by
cardiac arrhythmia, it is unclear if antiarrhythmics are bene-
ficial or detrimental in the postresuscitation period. Thus,
there is insufficient evidence to recommend for or against
prophylactic administration of antiarrhythmic drugs to pa-
tients who have survived cardiac arrest from any cause. It
may be reasonable, however, to continue an infusion of an
antiarrhythmic drug that was associated with ROSC (Class
Indeterminate). Also, given the cardioprotective effects of
H9252-blockers in the context of ischemic heart disease, the use of
H9252-blockers in the postresuscitation setting seems prudent if
there are no contraindications.
9
IV-86 Circulation December 13, 2005
Central Nervous System
A healthy brain and a functional patient are the primary goals
of cardio-pulmonary-cerebral resuscitation. Following
ROSC, after a brief initial period of hyperemia cerebral blood
flow is reduced (the “no-reflow phenomenon”) as a result of
microvascular dysfunction. This reduction occurs even when
cerebral perfusion pressure is normal.
43,44
Neurologic support for the unresponsive patient should
include measures to optimize cerebral perfusion pressure by
maintaining a normal or slightly elevated mean arterial
pressure and reducing intracranial pressure if it is elevated.
Because hyperthermia and seizures increase the oxygen
requirements of the brain, providers should treat hyperther-
mia and consider therapeutic hypothermia. Witnessed sei-
zures should be promptly controlled and maintenance anti-
convulsant therapy initiated (Class IIa). Because of a paucity
of data, routine seizure prophylaxis is a Class Indeterminate
recommendation at present.
Prognostic Factors
The period after resuscitation is often stressful to medical
staff and family members as questions arise about the
patient’s ultimate prognosis. Ideally a clinical assessment,
laboratory test, or biochemical marker would reliably predict
outcome during or immediately after cardiac arrest. Unfortu-
nately no such predictors are available. Determination of
prognosis based on initial physical examination findings can
be difficult, and coma scores may be less predictive than
individual motor and brainstem reflexes found in the first 12
to 72 hours after arrest.
2
In a meta-analysis (LOE 1)
44
bilateral absence of cortical
response to median nerve somatosensory-evoked potentials
predicted poor outcome in normothermic patients who were
comatose for at least 72 hours after hypoxic-ischemic insult.
A case report
46
also documents the usefulness of this evalu-
ation. Therefore, median nerve somatosensory-evoked poten-
tials measured 72 hours after cardiac arrest can be used to
predict neurologic outcome in patients with hypoxic-anoxic
coma.
A recent meta-analysis (LOE 1) of 11 studies involving
1914 patients
2
documented 5 clinical signs that were found to
strongly predict death or poor neurologic outcome, with 4 of
the 5 predictors detectable at 24 hours after resuscitation:
●
Absent corneal reflex at 24 hours
●
Absent pupillary response at 24 hours
●
Absent withdrawal response to pain at 24 hours
●
No motor response at 24 hours
●
No motor response at 72 hours
An electroencephalogram performedH1102224 to 48 hours after
resuscitation has also been shown to provide useful predictive
information (LOE 5
47–50
) and can help define prognosis.
Other Complications
Sepsis is a potentially fatal postresuscitation complication.
51
Patients with sepsis will benefit from goal-directed therapy.
Renal failure
52
and pancreatitis, while often transient, should
be diagnosed and evaluated.
3,53
Summary
The postresuscitation period is often marked by hemodynam-
ic instability as well as laboratory abnormalities. This is also
a period for which promising technological interventions
such as controlled therapeutic hypothermia are being evalu-
ated. Every organ system is at risk during this time, and
patients may ultimately develop multi-organ dysfunction. A
complete discussion of this topic is beyond the scope of this
chapter. The goal of the postresuscitation period is to manage
the patient’s vital signs and laboratory abnormalities and
support organ system function to increase the likelihood of
intact neurologic survival.
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