i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2

Available online at www.sciencedirect.com

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journal homepage: www.elsevier.com/locate/ihj

Review Article

Post-resuscitation care for survivors of cardiac

arrest

Ashvarya Mangla a, Mohamud R. Daya b, Saurabh Gupta c,d,e,*

a
Clinical Assistant Professor of Medicine, OSF Saint Francis Medical Center, University of Illinois College of Medicine,
Peoria, IL, USA
b
Associate Professor of Emergency Medicine, Oregon Health & Science University, Portland, OR, USA
c
Director, Cardiac Catheterization Laboratories, USA
d
Co-Director, Multi-Disciplinary Heart Valve Clinic, USA
e
Assistant Professor of Medicine, Oregon Health & Science University, Portland, OR, USA

article info abstract

Article history: Cardiac arrest can occur following a myriad of clinical conditions. With advancement of
Received 2 November 2013 medical science and improvements in Emergency Medical Services systems, the rate of
Accepted 4 December 2013 return of spontaneous circulation for patients who suffer an out-of-hospital cardiac arrest
Available online 10 January 2014 (OHCA) continues to increase. Managing these patients is challenging and requires a
structured approach including stabilization of cardiopulmonary status, early consideration
Keywords: of neuroprotective strategies, identifying and managing the etiology of arrest and initiating
Out-of-hospital cardiac arrest treatment to prevent recurrence. This requires a closely coordinated multidisciplinary
Return of spontaneous circulation team effort. In this article, we will review the initial management of survivors of OHCA,
Post-resuscitation care highlighting advances and ongoing controversies.
PCI Copyright ª 2014, Cardiological Society of India. All rights reserved.
Therapeutic hypothermia

cognitive function. Proper post-resuscitation care (PRC) has

1. Introduction
Cardiac arrest (CA) is often the terminal event following pro-
gression of and decompensation from a wide range of path-
ophysiological events. With medical advances and
improvements in the delivery of prehospital care, we are
witnessing increasing rates of return of spontaneous circula-
tion (ROSC) following CA. Once resuscitated, the next chal-
lenge is to manage these patients appropriately so as to not
only prevent mortality but preserve neurological and
been shown to reduce mortality and morbidity.1e3 To achieve
this, a closely coordinated multidisciplinary team effort is
required. The key steps involved in caring for these patients
include:
- Assessment and stabilization of cardiopulmonary status
- Determining etiology of arrest
- Neuroprotection
- Preventing recurrence of arrest.

* Corresponding author. UHN-62, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098, USA.
E-mail address: guptasa@ohsu.edu (S. Gupta).
0019-4832/$ e see front matter Copyright ª 2014, Cardiological Society of India. All rights reserved.
http://dx.doi.org/10.1016/j.ihj.2013.12.028
S106 i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2
All these steps generally must start simultaneously once
the patient regains a pulse. A schematic overview of managing
patients post-ROSC is outlined in Fig. 1.
2. Prehospital management
After ROSC, (defined as a palpable pulse and recordable blood
pressure and if monitored, increase in ETCO2 of >40 mm of
Hg), emergency medical services (EMS) personnel should
transport patients to facilities equipped with managing the
complex needs of these patients. It may be safe to bypass
closer medical facilities and transport patients to institutions
capable of meeting the needs for PRC.4e6 Prior to and during
transport, intravenous access should be established and cir-
culation, airway and breathing (CAB) supported in accordance
with basic and advanced cardiac life support guidelines. If
possible, a 12-lead electrocardiogram (ECG) should be ob-
tained. If the field ECG is consistent with a ST-segment
elevation myocardial infarction (STEMI), the cardiac cathe-
terization team at the receiving facility should be alerted.
Although some EMS systems currently initiate therapeutic
hypothermia (TH) for neuroprotection in patients who remain
comatose post-ROSC, there is lack of conclusive evidence of
improvements in outcomes when compared to delayed initi-
ation of hypothermia in the ED.7 Until, further evidence be-
comes available, the strategy of prehospital post-resuscitation
hypothermia cannot be routinely recommended.
3. Emergency Department (ED) management
Initial management of patients post-ROSC involves a multi-
system approach8 and should focus on several key areas
simultaneously:
- Adequate ventilation and oxygenation
- Hemodynamic optimization
- Cardiovascular stabilization
- Management of metabolic derangements
- Determining the etiology and initiating treatment of the
etiology of arrest
- Neurological assessment and consideration of therapeutic
hypothermia.
Upon arrival in ED, patient’s cardiopulmonary and neuro-
logical status should be promptly assessed. Continuous car-
diac monitoring, pulse oximetry, capnography and NIBP (non-
invasive blood pressure) monitoring should be initiated. This
provides critical information on tissue oxygenation and
perfusion and helps guide further resuscitative care.
A brief and focused history should be obtained if feasible.
Since most patients may be unable to communicate, this may
need to be obtained from EMS personnel, family, friends or
bystanders who have witnessed the arrest. Up to 80% of pa-
tients have symptoms preceding the arrest.9 Historical evi-
dence of chest pain, shortness of breath, palpitations, light
headedness, abdominal pain, back pain, recent infection, loss
of postural tone, focal neurological deficits, seizures, and ev-
idence of trauma or bleeding may provide clues to specific
etiologies. Information should also be obtained about past
medical history, recent travel, medications, known allergies
and whether patients were eating at the time of arrest.
A focused physical examination should be performed in
the ED. Pupils should be checked for size, symmetry and
response to light. Lungs should be assessed for ventilation
adequacy. Stridor and wheezing may point to underlying
upper or lower airway obstruction and asymmetric breath
sounds should raise concern for an associated pneumothorax
(PTX). Cardiac examination should focus on identifying dys-
rhythmias, adequacy of circulation assessed by blood pres-
sure and pulse strength in all 4 limbs. Presence of cardiac
murmurs should be noted. Low intensity or distant heart
sounds should prompt consideration for underlying pericar-
dial tamponade. Abdomen should be assessed for evidence of
distension, guarding or presence of pulsatile masses. Rectal
exam should be considered to evaluate for gastrointestinal
bleeding. The patient should also be assessed for complica-
tions related to cardiopulmonary resuscitation (CPR).
All patients presenting with ROSC should undergo a thor-
ough and detailed neurological exam to evaluate mental sta-
tus (using a validated scale such as the Glasgow Coma Score
(GCS)) and identify focal neurological findings. Patients who
remain comatose (unable to follow verbal commands or a GCS
of 8) and whose first recorded rhythm was ventricular
fibrillation (VF) benefit from Therapeutic Hypothermia (TH)
and this should be initiated as soon as feasible.10,11
3.1. Initial workup
The workup should focus on assessing organ function and
identifying underlying causes (Table 1).
- A basic metabolic panel including a magnesium level can
identify electrolyte abnormalities,12 a complete blood
count with differential may aid in identifying infection or
anemia. An arterial blood gas (ABG) permits assessment for
acidosis, hypoxia and hypercapnea while providing feed-
back on ventilatory status. Serum lactate levels are helpful
to assess tissue perfusion. Resuscitated patients with
elevated lactate levels require serial measurements;
greater lactate clearance at 24 h is associated with
improved survival.13 Baseline coagulation tests and cardiac
biomarkers (troponin, CPK-MB) may be obtained and seri-
ally followed as needed though the utility of initial
troponin levels in directing initial management of patients
post-ROSC remains unclear.14 Toxicology testing can be
considered in selected cases, although results rarely
change initial management. When available, point-of-care
testing should be utilized to expedite clinical decision
making.
- A 12-lead ECG should be analyzed in all patients with CA
for presence of ST-segment deviation, T-wave abnormal-
ities, dysrhythmias, conduction defects, QT-interval and
presence of low voltage (which may indicate tamponade).8
An initial as well as repeat 12-lead ECG’s are critical for
early recognition of ongoing myocardial ischemia and
presence of arrhythmias that require treatment. A 64-lead
continuous ST mapping obtained using a chest vest may
enhance sensitivity and specificity compared to a standard
 i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2 S107

Fig. 1 e Algorithm highlighting the important pathways involved in caring for patient with ROSC post-cardiac arrest. ROSC e
return of spontaneous circulation; CAB e circulation, airway, breathing; ECG e electrocardiogram; iv e intravenous, SBP e
systolic blood pressure; MAP e mean arterial pressure; PCI e percutaneous coronary intervention; ET e endotracheal; K e
potassium; Ed e Emergency Department, ICU e intensive care unit. * Can keep FIO2 of 100% in case of carbon monoxide or
cyanide poisoning.
S108 i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2

 Electroencephalogram (EEG): Status epilepticus can lead

Table 1 e Common causes of cardiac arrest.
to CA and non-convulsive status epilepticus (NCSE) is
Cardiovascular Acute coronary syndromes often seen post-arrest.18 Continuous EEG has a high
causes Arrhythmias
sensitivity for detecting this and should be performed as
Structural heart disease: Hypertrophic
soon as feasible in comatose patients.8 Patients under-
cardiomyopathy, ARVD
Cardiac tamponade going TH should have continuous EEG monitoring to
Aortic dissection or aortic aneurysm rupture detect seizures and to help differentiate seizures from
Blunt cardiac trauma: commotio cordis hypothermia induced shivering.
Pulmonary Pulmonary embolism
causes Status asthmaticus 3.2. Ventilation
Airway obstruction : foreign body, mucus
plugging
Following resuscitation, the airway should be assessed to
Pneumothorax
ensure adequate oxygenation and ventilation in all patients. A
Hypoxia
Electrolyte Hypokalemia/hyperkalemia safe airway should be established and comatose patients
abnormalities Hypomagnesemia intubated (if not done prior to arrival). Mechanical ventilator
Hypocalcemia/hypercalcemia settings should be adjusted as needed based on ABG results.
Acidosis Patients who develop ARDS should be managed with low tidal
Renal failure volume ventilation with PEEP adjusted to keep plateau pres-
Infection Sepsis
sures 30 cm of H2O.21
Hypovolemia Bleeding
Awake patients with appropriate respiratory effort and
Gastrointestinal losses
Diuretic therapy able to maintain their airway can be monitored without
Toxins Cocaine abuse intubation. Controlled use of supplemental oxygen to achieve
Amphetamines SpO2 94% is recommended in the non-intubated patients
Opiate overdose post-resuscitation. Similarly, in patients who are intubated
Cardio active agents FIO2 should be quickly titrated to maintain SpO2 94%. Higher
Benzodiazepine overdose
PaO2 levels may lead to adverse neurological outcomes sec-
Tricyclic antidepressants
ondary to generation of free radicals and brain lipid peroxi-
ARVD e arrhythmogenic right ventricular dysplasia. dation in the context of global ischemia followed by
reperfusion.8,19
12-lead ECG for detecting underlying coronary artery oc- PaCO2 should also be kept in normal range. Hyperventila-
clusion,15 however, additional studies are warranted prior tion can lead to decrease in PaCO2, and decrease cerebral
to recommending routine implementation of this strategy. perfusion leading to worsening of post-ischemic cerebral
- Imaging studies: injury.20 Additionally, hyperventilation decreases expiratory
 Chest X-Ray (CXR): A portable CXR can identify pulmo- time leading to air trapping and increase in intrathoracic
nary etiologies or complications such as pulmonary pressure. This impedes preload and decreases cardiac output
edema, PTX, pneumonia and verify correct positioning of which can be deleterious in hypotensive patients. Generally,
endotracheal tube patients who are intubated. PaCO2 should be maintained around 40e45 mm of Hg and, if
 CT: In comatose patients, non-contrast CT of brain may monitored, end-tidal CO2 (capnometry) level should be kept
help in early detection of underlying stroke as well as between 35e40 mm of Hg.8
cerebral edema. The presence of cerebral edema on CT
post-CA is associated with decreased survival.16 A CT of 3.3. Hemodynamic optimization
abdomen and pelvis should be considered in patients
with suspected abdominal etiology. A contrast chest CT Post-CA, it is essential to maintain perfusion to vital organs to
is helpful in the workup for suspected pulmonary em- prevent further clinical deterioration. Irrespective of the eti-
bolism (PE) or aortic dissection. ology of arrest, there may be temporary myocardial dysfunc-
 Echocardiography and Ultrasonography (US): Bedside tion and inability to maintain adequate cardiac output.22,23 For
echocardiography can be performed if there is suspicion optimal organ perfusion a MAP (mean arterial pressure)
of underlying cardiac ischemia and the initial ECG is non- 65 mm of Hg should be targeted. The first step in ensuring
diagnostic. Global hypokinesis is expected but regional this is adequate volume resuscitation with isotonic fluids
wall motion abnormalities suggest ischemia. In patients (0.9% normal saline or ringer’s lactate) to achieve a central
with suspected PE who cannot undergo CT, echocardio- venous pressure of 8e12 cm of H2O. Cold saline may be used
graphic evidence of right ventricular dysfunction or in for volume loading if TH is being considered. If, after adequate
some instances direct visualization of clot can confirm volume supplementation (usually 2e3 L of isotonic fluids), the
the diagnosis. Pericardial tamponade and structural MAP remains <60e65 mm of Hg; vasopressors and inotropic
heart diseases such as hypertrophic cardiomyopathy can agents should be added. The available agents include
also be identified rapidly through bedside echocardiog- norepinephrine, dopamine, epinephrine, phenylephrine,
raphy. In addition, US can be used to assess for presence dobutamine and milrinone. There is paucity of data to defin-
of PTX, pulmonary edema, intra-abdominal bleeding, itively recommend one agent and choice of agents should be
and volume status based on the size of inferior vena dictated by goals of therapy, side effects and familiarity of
cava.17 providers. While optimization is underway, hemodynamic
 i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2
parameters should be monitored frequently through periodic
NIBP monitoring or, in some instances invasive direct arterial
pressure monitoring.
3.4. Cardiovascular stabilization and role of coronary
angiography
Coronary artery occlusion remains a leading cause of out-of-
hospital cardiac arrest (OHCA).24,25 An initial 12-lead ECG
should be obtained in all patients post-arrest.8 If STEMI is
noted, reperfusion therapy should be strongly considered:
either via primary percutaneous coronary intervention (PCI)
or intravenous fibrinolytic therapy as both have been shown
to be efficacious.26 Traumatic or prolonged CPR (>10 min) is a
relative contraindication to fibrinolytic use27 and the risk and
benefits of fibrinolysis should be considered in this sub-group.
PCI can be safely performed in patients undergoing TH28 but
the safety of fibrinolytic therapy for STEMI in conjunction with
TH is less well established. Preliminary studies suggest that
the risk of stent thrombosis is no different in patients treated
with or without TH.29 Consideration may be given to per-
forming angiography (and possible PCI) in all patients
following ROSC who do not have an alternate explanation of
arrest irrespective of the ECG findings30,31 but the benefit of
routinely implementing this approach remains controversial
and it has been challenging to identify patients who would
benefit most from invasive assessment and treatment. Future
research should be directed towards developing modalities
identifying these patients appropriately. Body surface poten-
tial mapping as mentioned previously is one such modality.15
Continuous cardiac monitoring should be performed in all
patients to monitor for arrhythmias in the post-arrest period.
When detected, arrhythmias should be managed as appro-
priate per current resuscitation guidelines.8 Patients with MI
who continue to be hypotensive despite revascularization
may need mechanical augmentation with devices such as
intra-aortic balloon pump or percutaneous mechanical cir-
culatory support in addition to vasoactive agents and fluids
provided no contraindications exist.
3.5. Therapeutic hypothermia
Neurological injury is a major cause of death following suc-
cessful resuscitation.32 Post-resuscitation TH has been
demonstrated to improve neurological outcomes in comatose
patients whose initial recorded rhythm was VF.10,11 Harmful
pathways that accompany reperfusion injury seem to be
inhibited by hypothermia and exacerbated by hyperthermia.
According to the 2010 AHA guidelines,8 all comatose patients
with ROSC after out of hospital VF arrest should be cooled to
32  Ce34  C for 12e24 h. TH should be considered for coma-
tose patients with ROSC after in-hospital CA from any rhythm
or OHCA from PEA or Asystole. Active rewarming is contra-
indicated in patients who develop spontaneous hypothermia
(temperature >32  C) after ROSC post-CA within the first 48 h.
TH should be induced as soon as possible, preferably
within 6 h of CA based on animal studies. TH can be induced
using cold saline infusion,7 endovascular33 or surface cooling
devices.34 Unintentional overcooling should be avoided. All
hospitals should establish standardized protocols for
S109
initiation and management of TH based on local logistics and
staff training.
During initiation and maintenance of TH, core body tem-
perature should be monitored continuously using esophageal
probe, bladder temperature catheter in non-anuric patients or
central venous probe.10,11 Axillary, oral, tympanic and rectal
temperatures can differ from core body temperature and
should be avoided.8 Shivering has an adverse impact on
maintenance of hypothermia and patients should be sedated
and if needed administered paralytics to avoid this compli-
cation of TH.
Important complications of TH include increased suscep-
tibility to infections,11,35 bleeding,34 electrolyte depletion,
bradyarrhythmias and hyperglycemia.36 Appropriate pre-
cautions should be taken to prevent infections and when
appropriate, antibiotics initiated. Frequent electrolyte moni-
toring should be performed during TH37 and appropriate he-
modynamic support maintained. Insulin therapy may be
required to prevent hyperglycemia.
Rewarming post-TH should be gradual and not exceed
0.5  C/h as rapid rewarming can lead to cerebral edema,
hyperkalemia and seizures.
3.6. Glycemic control
Unless hypoglycemia is the cause of arrest, post-arrest pa-
tients usually demonstrate hyperglycemia. Hyperglycemia is
detrimental38 and impairs neurological recovery.39 Optimal
blood glucose range in patients post-CA remains unknown but
strict normoglycemia is not required.40 Strict blood sugar
control with intensive insulin therapy targeting values lower
than 110 mg/dl can lead to hypoglycemia41 which has been
associated with increased mortality.42 Additionally, strict
glucose control compared with moderate glucose control has
not been shown to confer any mortality benefit in these pa-
tients.43 Thus, moderate glycemic control (144e180 mg/dl) is
preferred and insulin therapy should be targeted to this goal.8
3.7. Management of specific etiology of arrest
Table 2 briefly summarizes management of common etiol-
ogies of CA.
4. Neuroprognostication
Neuroprognostication in patients post-CA is clinically chal-
lenging. While it’s important to guide medical decision mak-
ing regarding withdrawal of care, no single test reliably
predicts poor outcomes, especially in the first 24 h post-ar-
rest.8 Generally, multiple independent prognosticators should
be used to assess the severity of neurological damage.44 Prior
to attempting neuroprognostication, any potential con-
founding factors such as hypotension, seizures, toxins or
neuromuscular blockers should be excluded. The exact timing
of neuroprognostication in patients who have undergone TH
remains unknown.45 According to 2010 AHA recommenda-
tion, all neuroprognostication efforts should be avoided in the
first 72-h post-arrest in patients treated with TH.8 In patients
S110 i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2

Findings on neuroimaging are less well defined but loss of

Table 2 e Management of common causes of cardiac
gray white matter interface and diffuse ischemia on CT or MRI
arrest.
are associated with poor prognosis.8,44
Acute coronary Coronary revascularization: PCI/fibrinolytic
Biomarkers such as Neuron Specific Enolase and S100-B
syndrome therapy
have been evaluated for prognostication in patients post-CA.
Hypoxia Management of underlying etiology,
supportive mechanical ventilation Elevated levels of these biomarkers have been associated with
(if needed) poor prognosis but there is variability and lack of standardi-
Pulmonary Anticoagulation, consideration should zation in these studies.44 Sole reliance on biomarkers for
embolism be given to fibrinolysis and thrombectomy. neuroprognostication is not recommended at this time.8
Electrolyte Hypokalemia: Supplementation
abnormalities Hyperkalemia: Calcium chloride/calcium
gluconate, sodium bicarbonate, albuterol
nebulizers, sodium polystyrene sulfonate
5. Preventing re-arrest
or diuresis as may be appropriate clinically
Hypomagnesemia: intravenous magnesium The most important measure to prevent re-arrest is identi-
supplementation (always use in hypokalemic fying and treating the etiology of initial arrest. If any further
patients) episodes of CA occur while the patient is being monitored,
Acidosis: Reverse underlying cause, consider
then they should be treated with CPR, defibrillation, vaso-
bicarbonate for patients with severe metabolic
pressors and antiarrhythmic therapy as appropriate. At this
acidosis
Hypoglycemia: intravenous dextrose time evidence is insufficient to routinely recommend or refute
Cardiac Pericardiocentesis using antiarrhythmic agents prophylactically.8
tamponade
Pneumothorax Needle thoracostomy followed by chest tube
insertion 6. Role of specialized centers
Anaphylaxis Epinephrine
Toxins Use of antidotes as appropriate.
Managing patients post-CA involves a team based approach
Anemia/ Isotonic crystalloid fluids, packed RBCs.
hypovolemia and requires complex coordination of care including acute he-
Severe Gentle rewarming modynamic stabilization, management of mechanical venti-
hypothermia lation, consideration of TH and interventions such as emergent
Stroke Revascularization for ischemic stroke PCI. These objectives are best achieved at centers having
depending on timing, consideration to expertise in dealing with this complex subset of patients. Cen-
neurosurgical decompression for
ters dealing with larger volume of post-CA patients have been
hemorrhagic stroke.
shown to have superior outcomes5 and lower in-hospital mor-
tality rates.49 Regional centers for care of patients who survive
not treated with TH, neuroprognostication can be considered CA have been proposed by international organizations4 and
24-h post-arrest. there is a need for local regulatory authorities to formulate and
Findings on neurological exam associated with poor implement an action plan to achieve this goal. CA can unfor-
prognosis in patients not undergoing TH include: absent tunately happen to anyone, and everyone should at-least get
corneal reflex at 24 h, absent pupillary reflex at 24 h, absent or the best possible shot at survival by implementation and utili-
withdrawal response to pain at 24 h and no motor response at zation of available evidence based therapies.
24 and 72 h.46 In patients undergoing TH, a score of 5 on GCS
motor scale (GCS-M) and normal brain stem reflexes have
been associated with favorable prognosis while a bilateral lack 7. Summary
of pupillary reflex, corneal reflex and a score of 1e2 on GCS-M
have been associated with unfavorable outcome.44 Management of patients following resuscitation from CA is
When available, somatosensory evoked potentials (SSEP) complex and requires specialized institutions capable of
can be helpful in neuroprognostication. Bilateral absence of providing advanced care therapies. Optimal management re-
N20 cortical response to median nerve stimulation on SSEP is quires consideration of multiple processes simultaneously. In
associated with poor prognosis.8,44 Results of SSEPs are not addition to CABs of advanced cardiac life support, neuro-
affected by sedation and preliminary results suggest that protection with TH should be initiated in comatose patients.
SSEPs may be useful in patients undergoing TH.44,47 The presence of coronary artery occlusion as a cause of arrest
No EEG finding can reliably predict poor outcome in first should be determined through analysis of the 12-lead ECG and
24 h post-arrest.8 In patients not treated with TH, an EEG when present, treated expeditiously. Patients should be moni-
showing generalized suppression to <20 mV, burst suppres- tored closely in a critical care setting and neuroprognostication
sion pattern associated with generalized epileptic activity or should be performed no earlier than 24 h in patients not un-
diffuse periodic complexes on flat background is associated dergoing TH and after 72 h in patients undergoing TH.
with poor outcome.8,48 In patients treated with TH, a reactive
or a continuous EEG background after rewarming is associated
with favorable prognosis while burst suppression pattern, Conflicts of interest
electro-cerebral inactivity or status epilepticus are associated
with unfavorable prognosis.44 All authors have none to declare.
 i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2 S111

references edema and outcome after cardiac arrest. Resuscitation.

2011;82:1180e1185.
17. Moore CL, Copel JA. Point-of-care ultrasonography. N Engl J
Med. 2011;364:749e757.
1. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest
18. Rittenberger JC, Popescu A, Brenner RP, Guyette FX,
syndrome: epidemiology, pathophysiology, treatment, and
Callaway CW. Frequency and timing of nonconvulsive status
prognostication. A consensus statement from the
epilepticus in comatose post-cardiac arrest subjects treated
International Liaison Committee on Resuscitation (American
with hypothermia. Neurocrit Care. 2012;16:114e122.
Heart Association, Australian and New Zealand Council on
19. Kilgannon JH, Jones AE, Parrillo JE, et al. Relationship between
Resuscitation, European Resuscitation Council, Heart and
supranormal oxygen tension and outcome after resuscitation
Stroke Foundation of Canada, InterAmerican Heart
from cardiac arrest. Circulation. 2011;123:2717e2722.
Foundation, Resuscitation Council of Asia, and the
20. Yundt KD, Diringer MN. The use of hyperventilation and its
Resuscitation Council of Southern Africa); the American
impact on cerebral ischemia in the treatment of traumatic
Heart Association Emergency Cardiovascular Care
brain injury. Crit Care Clin. 1997;13:163e184.
Committee; the Council on Cardiovascular Surgery and
21. Network A. Ventilation with lower tidal volumes as compared
Anesthesia; the Council on Cardiopulmonary, Perioperative,
with traditional tidal volumes for acute lung injury and the
and Critical Care; the Council on Clinical Cardiology; and the
acute respiratory distress syndrome. N Engl J Med.
Stroke Council. Circulation. 2008;118:2452e2483.
2000;342:1301e1308.
2. Safar P. Resuscitation from clinical death: pathophysiologic
22. Laurent I, Monchi M, Chiche JD, et al. Reversible myocardial
limits and therapeutic potentials. Crit Care Med.
dysfunction in survivors of out-of-hospital cardiac arrest. J
1988;16:923e941.
Am Coll Cardiol. 2002;40:2110e2116.
3. Sunde K, Pytte M, Jacobsen D, et al. Implementation of a
23. Ruiz-Bailen M, Aguayo de Hoyos E, Ruiz-Navarro S, et al.
standardised treatment protocol for post resuscitation care
Reversible myocardial dysfunction after cardiopulmonary
after out-of-hospital cardiac arrest. Resuscitation.
resuscitation. Resuscitation. 2005;66:175e181.
2007;73:29e39.
24. Spaulding CM, Joly LM, Rosenberg A, et al. Immediate
4. Nichol G, Aufderheide TP, Eigel B, et al. Regional systems of
coronary angiography in survivors of out-of-hospital cardiac
care for out-of-hospital cardiac arrest: a policy statement
arrest. N Engl J Med. 1997;336:1629e1633.
from the American Heart Association. Circulation.
25. Anyfantakis ZA, Baron G, Aubry P, et al. Acute coronary
2010;121:709e729.
angiographic findings in survivors of out-of-hospital cardiac
5. Callaway CW, Schmicker R, Kampmeyer M, et al. Receiving
arrest. Am Heart J. 2009;157:312e318.
hospital characteristics associated with survival after out-of-
26. Voipio V, Kuisma M, Alaspaa A, Manttari M, Rosenberg P.
hospital cardiac arrest. Resuscitation. 2010;81:524e529.
Thrombolytic treatment of acute myocardial infarction after
6. Spaite DW, Stiell IG, Bobrow BJ, et al. Effect of transport
out-of-hospital cardiac arrest. Resuscitation. 2001;49:251e258.
interval on out-of-hospital cardiac arrest survival in the
27. O’Connor RE, Brady W, Brooks SC, et al. Part 10: acute
OPALS study: implications for triaging patients to specialized
coronary syndromes: 2010 American Heart Association
cardiac arrest centers. Ann Emerg Med. 2009;54:248e255.
Guidelines for Cardiopulmonary Resuscitation and
7. Bernard SA, Smith K, Cameron P, et al. Induction of
Emergency Cardiovascular Care. Circulation.
therapeutic hypothermia by paramedics after resuscitation
2010;122:S787eS817.
from out-of-hospital ventricular fibrillation cardiac arrest: a
28. Batista LM, Lima FO, Januzzi Jr JL, Donahue V, Snydeman C,
randomized controlled trial. Circulation. 2010;122:737e742.
Greer DM. Feasibility and safety of combined percutaneous
8. Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: post-
coronary intervention and therapeutic hypothermia
cardiac arrest care: 2010 American Heart Association
following cardiac arrest. Resuscitation. 2010;81:398e403.
Guidelines for Cardiopulmonary Resuscitation and
29. Rosillo SO, Lopez-de-Sa E, Iniesta AM, et al. Is therapeutic
Emergency Cardiovascular Care. Circulation.
hypothermia a risk factor for stent thrombosis? J Am Coll
2010;122:S768eS786.
Cardiol. 2013, Oct 4. http://dx.doi.org/10.1016/
9. Muller D, Agrawal R, Arntz HR. How sudden is sudden cardiac
j.jacc.2013.09.028. pii:S0735-1097(13)05536-8 [Epub ahead of
death? Circulation. 2006;114:1146e1150.
print].
10. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose
30. Larsen JM, Ravkilde J. Acute coronary angiography in
survivors of out-of-hospital cardiac arrest with induced
patients resuscitated from out-of-hospital cardiac arrest-a
hypothermia. N Engl J Med. 2002;346:557e563.
systematic review and meta-analysis. Resuscitation.
11. Group. HaCAS. Mild therapeutic hypothermia to improve the
2012;83:1427e1433.
neurologic outcome after cardiac arrest. N Engl J Med.
31. Dumas F, Cariou A, Manzo-Silberman S, et al. Immediate
2002;346:549e556.
percutaneous coronary intervention is associated with better
12. Gettes LS. Electrolyte abnormalities underlying lethal and
survival after out-of-hospital cardiac arrest: insights from the
ventricular arrhythmias. Circulation. 1992;85:I70eI76.
PROCAT (Parisian Region Out of hospital Cardiac ArresT)
13. Donnino MW, Miller J, Goyal N, et al. Effective lactate
registry. Circ Cardiovasc Interv. 2010;3:200e207.
clearance is associated with improved outcome in post-
32. Laver S, Farrow C, Turner D, Nolan J. Mode of death after
cardiac arrest patients. Resuscitation. 2007;75:229e234.
admission to an intensive care unit following cardiac arrest.
14. Dumas F, Manzo-Silberman S, Fichet J, et al. Can early cardiac
Intensive Care Med. 2004;30:2126e2128.
troponin I measurement help to predict recent coronary
33. Al-Senani FM, Graffagnino C, Grotta JC, et al. A prospective,
occlusion in out-of-hospital cardiac arrest survivors? Crit Care
multicenter pilot study to evaluate the feasibility and safety
Med. 2012;40:1777e1784.
of using the CoolGard System and Icy catheter following
15. Daly MJ, Finlay DD, Scott PJ, Nugent CD, Adgey AA,
cardiac arrest. Resuscitation. 2004;62:143e150.
Harbinson MT. Pre-hospital body surface potential mapping
34. Jarrah S, Dziodzio J, Lord C, et al. Surface cooling after cardiac
improves early diagnosis of acute coronary artery occlusion
arrest: effectiveness, skin safety, and adverse events in
in patients with ventricular fibrillation and cardiac arrest.
routine clinical practice. Neurocrit Care. 2011;14:382e388.
Resuscitation. 2013;84:37e41.
35. Perbet S, Mongardon N, Dumas F, et al. Early-onset
16. Metter RB, Rittenberger JC, Guyette FX, Callaway CW.
pneumonia after cardiac arrest: characteristics, risk factors
Association between a quantitative CT scan measure of brain
S112 i n d i a n h e a r t j o u r n a l 6 6 ( 2 0 1 4 ) s 1 0 5 es 1 1 2
and influence on prognosis. Am J Respir Crit Care Med.
2011;184:1048e1054.
36. Cueni-Villoz N, Devigili A, Delodder F, et al. Increased blood
glucose variability during therapeutic hypothermia and
outcome after cardiac arrest. Crit Care Med.
2011;39:2225e2231.
37. Polderman KH, Peerdeman SM, Girbes AR.
Hypophosphatemia and hypomagnesemia induced by
cooling in patients with severe head injury. J Neurosurg.
2001;94:697e705.
38. Langhelle A, Tyvold SS, Lexow K, Hapnes SA, Sunde K,
Steen PA. In-hospital factors associated with improved
outcome after out-of-hospital cardiac arrest. A comparison
between four regions in Norway. Resuscitation.
2003;56:247e263.
39. Mullner M, Sterz F, Binder M, Schreiber W, Deimel A,
Laggner AN. Blood glucose concentration after
cardiopulmonary resuscitation influences functional
neurological recovery in human cardiac arrest survivors. J
Cereb Blood Flow Metab. 1997;17:430e436.
40. Losert H, Sterz F, Roine RO, et al. Strict normoglycaemic blood
glucose levels in the therapeutic management of patients
within 12 h after cardiac arrest might not be necessary.
Resuscitation. 2008;76:214e220.
41. Arabi YM, Tamim HM, Rishu AH. Hypoglycemia with
intensive insulin therapy in critically ill patients:
predisposing factors and association with mortality. Crit Care
Med. 2009;37:2536e2544.
42. Krinsley JS, Grover A. Severe hypoglycemia in critically ill
patients: risk factors and outcomes. Crit Care Med.
2007;35:2262e2267.
43. Oksanen T, Skrifvars MB, Varpula T, et al. Strict versus
moderate glucose control after resuscitation from ventricular
fibrillation. Intensive Care Med. 2007;33:2093e2100.
44. Cronberg T, Brizzi M, Liedholm LJ, et al. Neurological
prognostication after cardiac arrest e recommendations from
the Swedish Resuscitation Council. Resuscitation.
2013;84:867e872.
45. Perman SM, Kirkpatrick JN, Reitsma AM, et al. Timing of
neuroprognostication in postcardiac arrest therapeutic
hypothermia. Crit Care Med. 2012;40:719e724.
46. Booth CM, Boone RH, Tomlinson G, Detsky AS. Is this patient
dead, vegetative, or severely neurologically impaired?
Assessing outcome for comatose survivors of cardiac arrest. J
Am Med Assoc. 2004;291:870e879.
47. Bouwes A, Binnekade JM, Kuiper MA, et al. Prognosis of coma
after therapeutic hypothermia: a prospective cohort study.
Ann Neurol. 2012;71:206e212.
48. Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S. Practice
parameter: prediction of outcome in comatose survivors after
cardiopulmonary resuscitation (an evidence-based review):
report of the Quality Standards Subcommittee of the
American Academy of Neurology. Neurology. 2006;67:203e210.
49. Carr BG, Kahn JM, Merchant RM, Kramer AA, Neumar RW.
Inter-hospital variability in post-cardiac arrest mortality.
Resuscitation. 2009;80:30e34.