UHM 2016, Vol. 43, No.

1 CARDIAC ARREST IN THE HYPERBARIC ENVIRONMENT: CASE REPORTS

Treatment of cardiac arrest in the hyperbaric environment:

key steps on the sequence of care case reports
K.T. Wright, S.P. Praske, N.A. Bhatt, R.M. Magalhaes, T.M. Quast
U.S. Naval Hospital Guam, Agana Heights, Guam
CORRESPONDING AUTHOR: Kevin T. Wright kevin.t.wright22.mil@mail.mil
______________________________________________________________________________________________________________________________________________________

ABSTRACT

The U.S. territory of Guam attracts thousands of

military and civilian divers annually and is home to
the only recompression facility within a 5,000-km
radius that accepts critically injured dive casualties.
As recompression chambers are confined spaces
and standard use of electrical cardioversion cannot
be used, cardiac resuscitation at depth must deviate
from advanced cardiovascular life support (ACLS)
algorithms. Furthermore, many hyperbaric chambers
that accept dive casualties are in remote locations,
a situation that requires providers to approach cardiac resuscitation in a different way when compared
to an in-hospital or ICU setting. This presents a

challenge to trained medical and diving professionals.

We present two contrasting vignettes of diving injuries initially responsive to appropriate treatment
but then deteriorating during recompression therapy
and ultimately requiring resuscitation at depth.
Additionally, we explore the physiologic basis of
resuscitation in a hyperbaric environment as it
relates to the treatment of cardiac arrest at depth.
This review critically examines the current guidelines in place for emergency cardiac resuscitation
in a hyperbaric chamber followed by recommendations for the key steps in the sequence of care.

______________________________________________________________________________________________________________________________________________________

INTRODUCTION
Carrying out current resuscitation guidelines in a
timely fashion is challenging in the hyperbaric setting
for the following reasons: (i) the physical constraints
related to the hyperbaric chamber; (ii) initial cardiopulmonary resuscitation (CPR) in most cases can be
provided only by a single responder; and (iii) the
delay in initiating advanced therapeutic interventions
due to decompression safety requirements.
On the other hand, the hyperbaric, hyperoxic environment may theoretically delay the onset of hypoxia.
Additionally, most cardiac arrests that occur in the
hyperbaric setting are witnessed and responded to
immediately by trained medical personnel.
We present two contrasting vignettes of dive injuries
that highlight the challenges of cardiac resuscitation at
depth. Additionally, we explore the physiologic basis of
resuscitation in a hyperbaric environment as it relates to
the treatment of cardiac arrest at depth.

This review highlights the unique challenges of conducting emergency cardiac resuscitation in a hyperbaric chamber in Guam, home to the only recompression facility within a 5,000-km radius that
accepts critically injured dive casualties.
Scope of review
This review addresses the course of action recommended in the sequence of care for cardiac arrest in a
hyperbaric chamber at 60 and 30 feet sea water (fsw)
(183.8 and 91.9 kPa), as these are the most common
treatment depths used during a U.S. Navy Treatment
Table 6 (TT6) (Figure 1). The principal audience is
for recompression chambers in isolated or austere environments, with limited manning and resources. This
review does not apply to facilities that utilize two inside tenders for dual-provider resuscitation on initial response, or those that have the option of defibrillation at
treatment depth. Step-by-step resuscitation algorithms

_______________________________________________________________________________________________________________________

KEYWORDS: cardiac arrest, hyperbaric oxygen, hyperbaric environment

Copyright 2016 Undersea & Hyperbaric Medical Society, Inc.

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UHM 2016, Vol. 43, No. 1 CARDIAC ARREST IN THE HYPERBARIC ENVIRONMENT: CASE REPORTS
Depth/Time Profile
0
15

depth
30

(fsw)

45

descent rate
20 ft/min

60

20

5 20

5 20 5

ascent rate
1 ft/min

ascent rate
1 ft/min

30 15

60

15

60

30

time at depth (minutes)

breathing media
O2

air

total elapsed time:

285 minutes
(not including
descent time)

Photo 1: The Naval Base Guam hyperbaric

chamber team at work.

Figure 1: U.S. Navy Treatment Table 6 (TT6)

TT6 is currently considered the standard of care for the
treatment of the majority of decompression illness cases

are not discussed, as this remains highly dependent

on the specific chamber, the clinical situation and the
proximity and quality of available medical expertise.
Definition of terms
For the purpose of this review a cardiac arrest is
any primary cardiovascular process that results in the
cessation of forward blood flow from the heart. An
inside tender is any medical provider with training
specific for patient care in a hyperbaric environment.
This is appropriate, as the majority of multiplace recompression chambers that accept and treat dive casualties have organic medical assets that include a trained
inside tender who is responsible for direct patient care
throughout the duration of hyperbaric treatments.
As a basis for discussion, this paper will refer to the
recommendations contained in the U.S. Navy Dive
Manual Revision 6 for resuscitation of a pulseless
diver, section 20-2.3: specifically, that defibrillation is
not currently authorized at depth; and second, if an
inside tender is outside the no-decompression limits
he/she should not be brought directly to the surface with
the patient in cardiac arrest [1].
METHODS
The key steps in the sequence of care for resuscitation
of a diver in cardiac arrest are defined and examined
separately. The cases were chosen for relevance to the
topic being discussed. All patient treatments were
conducted in a standard RCF-6500 dual-lock recompression facility as described in the U.S. Navy Dive
Manual (Photo 1).

72

Clinical relevance
The recompression facility at Naval base Guam has
conducted more than 500 documented treatments
(Figure 2) and in the last decade alone has accepted
and cared for 64 severely injured patients (intubated,
vital signs instability, central nervous system involvement), 10 of whom had a requirement for cardiac resuscitation immediately before or during recompression
therapy.
We present a small but illustrative experience with
two cases of cardiac arrest in a hyperbaric environment
in which, after extended resuscitation efforts, both
patients eventually succumbed to their injuries.
Although our database of dive accidents goes back
decades, a review of these accidents suggests that these
two relatively contemporary ones well illustrate what
one would encounter in a modern situation. A historical
review of all of these cases is not felt to be warranted
to demonstrate the authors point hereafter. Standard
of care for events leading up to the cardiac arrest
were based on the U.S. Navy Dive Manual guidelines for recompression therapy, as well as best
practices from that period of time.
Case 1
A 27-year-old male presented complaining of bilateral
lower extremity pain and weakness after completing
three scuba night dives. Within one hour of surfacing,
the patient noted bilateral leg pain and weakness with
an inability to stand in addition to full-body numbness,
dizziness and nausea. Prior to transfer a computerized
tomography (CT) scan had been performed at the local
civilian hospital, which showed gas in the great vessels
and no pneumothorax. The patient was recompressed

Wright KT, Praske SP, Bhatt NA, et al.

UHM 2016, Vol. 43, No. 1 CARDIAC ARREST IN THE HYPERBARIC ENVIRONMENT: CASE REPORTS
Recompression cases on Guam
90
80
number of patients

70
60
50
40
30
20
10
2013

2011

2009

2007

2005

2003

2001

1999

1997

1995

1993

1991

1989

1987

1985

1983

1981

1979

year
patients with documented treatments

to 60 fsw, and reported immediate improvement in

symptoms, which guided the decision to utilize a TT6
with maximum extensions. After five oxygen (O2)
breathing periods at 60 fsw, a completely normal neurological exam was documented. During the third O2
period at 30 fsw the patient suddenly became unresponsive. Bag valve mask ventilations were immediately
started and shortly thereafter the patient was pulseless. Chest compressions were initiated and three doses
of 1 mg of epinephrine were given every three to five
minutes. The patient was moved to the outer lock for
decompression, CPR was continued, and then the
patient was transferred to the surface. Once on the
surface, the patient was placed on a monitor and
asystole was noted. The patient was intubated successfully, CPR continued, and two more rounds of
epinephrine at a dose of 1 mg each, at two-minute
intervals were given. An ambulance was called and
the patient was transported to Naval Hospital where he
was pronounced dead from sudden cardiac death as
a result of severe decompression sickness.
Case 2
A 43-year-old male presented following a deep dive
complaining of abdominal pain and mental status
changes. Three minutes after surfacing, he noted severe
abdominal pain, became incoherent, and experienced

Wright KT, Praske SP, Bhatt NA, et al.

critically injured patients

bowel and bladder incontinence. He was diagnosed

with severe Type II decompression sickness (DCS) vs.
arterial gas embolism (AGE), and emergently recompressed to 60 fsw in the chamber. At the end of the
second O2 period, the diver remained tachypneic,
hypotensive, tachycardic, and his mental status remained impaired suggesting neurogenic shock. After
fluid resuscitation, the patient was comfortable and
vital signs and mentation had improved. However,
by the fifth O2 period at 60 fsw, his sensorium was
again impaired and during ascent to 30 fsw he became
severely tachypneic. The patient was emergently recompressed to 60 fsw without noticeable improvement
in symptoms. He developed seizures necessitating
bag valve mask ventilation, followed by cardiac arrest. Chest compressions were initiated, and the patient
was transferred to the outer lock and then on to the
surface. Asystole was noted, CPR was continued and
the patient was emergently transferred by ambulance
to Naval Hospital where he was pronounced dead
upon arrival. The attending physicians assessment was
that the patient succumbed to decompression sickness
Type II, severe, with pulmonary decompression. The
spinal cord and brain were felt to be involved, and
pulmonary edema was evaluated to have contributed
to the patients demise.

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a cardiac arrest at depth, the patient should be brought
to the surface while compressions and ventilations are
conducted [1]. This makes clinical sense, as studies
show early initiation of CPR can increase the patients
chances of survival with a favorable long-term neurologic recovery [4,5]. Despite this, one hyperbaric
text refers to a grace period in which it is stated that
CPR can be postponed for several minutes in the hyperoxic environment because it is assumed that the
high dissolved oxygen concentration in the blood delays the onset of tissue hypoxia [6]. To the best of our
knowledge, this assumption has yet to be challenged.

Photo 2: Inside tenders perform CPR

in the limited space of the hyperbaric
chamber outer lock.

Evaluation of key steps in hyperbaric

cardiac arrest sequence of care
The American Heart Associations four-step chain
of survival concept has been promoted as a means
of optimizing survivability of cardiac arrests in a normobaric environment [2]. Better survival has been
associated with the first three links of the chain: notably, early access to emergency care, early CPR and
early defibrillation [3]. Unfortunately, these links are
difficult to perform in the hyperbaric environment.
During emergency response to a dive accident in
any austere location, intra-arterial lines and advanced
monitoring are extremely impractical. To mitigate
these concerns, our team cycles manual blood pressure, pulse oximetry and standard vitals every
30 minutes or more frequently if necessary. Monitors
are not authorized in recompression facilities that
do not have electrically inert penetrators, which
are an expensive addition to any hyperbaric chamber, and one that is not common in chambers set
up for emergency dive injuries in austere locations.
The grace period
The U.S. Navy Dive Manual states that if defibrillation is available on the surface within 20 minutes of

74

Compression-only cardiopulmonary resuscitation

(CO-CPR)
Cardiopulmonary resuscitation in the hyperbaric setting has traditionally consisted of chest compressions
initially interspersed with rescue breathing (Photo 2).
However, in a multicenter randomized trial a clinically
meaningful survival difference in favor of CO-CPR
over traditional CPR was found among patients whose
arrest was due to a cardiac cause (15.5% vs. 12.3%) [7].
In a realistic study on out-of-hospital cardiac arrest,
CO-CPR resulted in significantly better 24-hour postresuscitation neurologically normal survival (70% vs.
42%) compared to the standard 30:2 CPR model [8].
Furthermore, interrupting chest compressions causes
severe consequences. In a ventricular fibrillation (V
FIB) pig model it took two minutes of chest compressions to establish an adequate coronary perfusion
pressure, which was lost when compressions were interrupted. Despite restarting compressions, coronary
perfusion pressure remained negative after 30 seconds
and carotid flow reached only 25% of the basal value
[9]. On the other hand, based on an animal model,
if compressions are started immediately, cerebral
blood flow can be maintained at 60% of pre-arrest values
[10]. Finally, in a normobaric environment, CO-CPR
delivered more oxygen for up to four minutes post arrest
than a variety of compression to ventilation ratios [11].
Oropharyngeal airway (OPA)
The insertion of an OPA as part of the initial resuscitation may decrease the chances of subsequent pulmonary barotrauma, reduce atelectasis and consequent
right-to-left shunting, and allow for improved venti-

Wright KT, Praske SP, Bhatt NA, et al.

UHM 2016, Vol. 43, No. 1 CARDIAC ARREST IN THE HYPERBARIC ENVIRONMENT: CASE REPORTS

Photo 3: A dive medical Techician starts

an intravenous line on a patient inside
a hyperbaric chamber.

lation. One study found that passive ventilation with

an oral pharyngeal airway was associated with improved neurologically intact survival when compared
to bag valve mask ventilation [12]. Additionally, the
regular use of an OPA frees up the caregiver to focus
on performing effective chest compressions [13].
Positive-pressure ventilation with a bag valve mask
during an emergency ascent has the real potential to
cause barotrauma. On the contrary, passive ventilation
occurs with chest compressions as long as there is a
patent airway [14]. Precordial compressions in an
animal model generated a minute ventilation of 3 liters
per minute, and spontaneous gasping generated an
additional minute ventilation of 2 liters per minute
[15].
In humans, gasping is observed consistently during
cardiac arrest [15] and prolongs the effectiveness of
CO-CPR [16]. Furthermore, passive ventilation with
an oral pharyngeal airway was associated with improved neurologically intact survival when compared
to bag valve mask ventilation as it prevented hyperventilation [12].
Although the effectiveness of chest compressions
is highly dependent on the technique [17,18], the
overall physiologic benefits of CO-CPR combined
with a patent airway from use of an OPA will maximize
the delivery of oxygen and ultimately lead to better
patient outcomes, especially in the context of a single
first responder. This benefit would be further amplified
by the placement of a simple oxygen mask over the
OPA.

Wright KT, Praske SP, Bhatt NA, et al.

Epinephrine and antiarrhythmics

Current data suggest that intravenous drug therapy
as part of ACLS has no incremental benefit in out-ofhospital cardiac arrest [3]. Despite this, it is generally
agreed that epinephrine augments the chances of a
patient achieving return of spontaneous circulation
(ROSC). One study found that patients given epinephrine achieved ROSC far more often than those who
did not (18.5% vs. 5.7%) [19], while another found
an even more impressive difference (30% vs. 11%)
[20]. Early administration of epinephrine is also more
beneficial than later administration [21]. A single hyperbaric technician, under the direct supervision
of a physician, would be able to deliver epinephrine to a patient with a pre-existing intravenous line
(Photo 3). If ROSC was achieved early in resuscitation, it may prevent the need to bring the patient to
the surface altogether. This would allow the chamber
team to continue unabated with recompression.
Defibrillation
The delay from collapse to delivery of the first shock
is the single most important determinant of survival
[22]. Each minute that defibrillation is delayed
reduces the chance of eventual hospital discharge
by 8%-10% [23]. In several independent studies, use
of a defibrillator in eight minutes or less was strongly
associated with improved survival [3,4,24,25]. One
group studied episodes of sudden cardiac death as
recorded with an ambulatory electrocardiography
device and found the average period from cardiac
arrest to death was less than 10 minutes [23].
Defibrillators have a large capacitor and smallbrushed motor known to discharge and spark, which
is dangerous in a hyperbaric environment. The risk
of fire caused by voltaic arcing generated between
the paddles combined with leakage of oxygen from
around the patients respiratory circuit [26] presents
too great a risk of fire. Although some facilities do
have in-chamber defibrillation capabilities, the great
majority of recompression facilities throughout the
world lack the funding required to install and certify
such equipment. Thus, patients must be decompressed to the surface prior to defibrillation.
If the inside tender is outside of no-decompression
limits the U.S. Navy Dive Manual states that the pulse-

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UHM 2016, Vol. 43, No. 1 CARDIAC ARREST IN THE HYPERBARIC ENVIRONMENT: CASE REPORTS
Ultimately, the possible adverse consequences of
hyperoxia during and after ROSC are of less concern
when compared to the greater benefit from ongoing
hyperbaric treatment for decompression illness [25,
28,29].

Photo 4: A dive medical team performing

a hyperbaric chamber cardiac arrest drill.

less patient should not be brought directly to the surface from the treatment depth. In this scenario, one
must complete the decompression stops as appropriate
for the tender, or transfer the patient to an outer lock,
if available, while keeping the inside tender at the
original treatment depth. This movement of emergency personnel from the surface to the treatment
depth, as well as the transfer of patients between inner
lock, outer lock and the surface, consumes precious
minutes and must be avoided by maintaining the
inside tender in a no-decompression status.
Hyperoxic environments and ROSC
After successful resuscitation, or return of circulation, the provider must remain aware of the potential
for harm with hyperoxia from continued recompression therapy. Hyperoxia, defined as an arterial partial
pressure of oxygen (PaO2) greater than 300 mmHg,
after ROSC may be associated with increased inhospital mortality [25]. However, the only randomized
controlled trial comparing 30% fraction of inspired
oxygen (FiO2) to 100% FiO2 after ROSC found no
difference in survival [27]. Furthermore, it is known
that hypoxemia during and after ROSC is also harmful
[25], and that a higher PaO2 during CPR leads to improved rates of hospital admission [27]. Thus, emphasis should be placed on avoidance of hypoxemia.

76

Summary of recommendations
It remains critical that the inside tender be maintained
in a no-decompression status during treatments by
planning in advance for the regular cycling of personnel over the course of recompression therapy,
especially with severely injured patients. This will
allow the medical team to bring a pulseless patient
directly to the surface and vastly decrease the time to
defibrillation, thus increasing the chances of achieving
ROSC.
Based on our analysis, we strongly advise against
delaying chest compressions. During transit to the
surface, sufficient evidence and physiological principles
support early initiation of CO-CPR. Placement of
an oropharyngeal airway at the onset of arrest will
facilitate passive ventilation during apnea, minimize
atelectasis and help to avoid hyperventilation injury.
Epinephrine appears to increase the chance of
achieving ROSC and should be administered early.
Finally, the medical provider must take steps to minimize hypoxemia after a cardiac arrest, and throughout the continued recompression of patients who have
achieved ROSC.
CONCLUSION
Outcomes in hyperbaric emergencies are highly dependent on the clinical situation and the chamber being
utilized; thus it may not be realistic to create a single
universal hyperbaric ACLS-like protocol. However,
great effort should be taken to adapt current inhospital standard of monitoring and treatment to
the conditions in a hyperbaric unit. Regular practice
of pulseless diver drills (Photo 4) and utilization of
hyperbaric cardiac arrest recommendations should
decrease defibrillation times and increase intra-arrest
tissue oxygenation, subsequently improving patient
outcome. This may very well be the difference between success and failure in a hyperbaric cardiac
arrest.

Wright KT, Praske SP, Bhatt NA, et al.

UHM 2016, Vol. 43, No. 1 CARDIAC ARREST IN THE HYPERBARIC ENVIRONMENT: CASE REPORTS
Disclosures
All authors are employed by the United States Navy.
The content of this paper does not reflect the specific
views of the military. All members have no financial
disclosures. No funding was obtained and there are no
financial disclosures or conflicts of interest to report.

Disclaimer
The views expressed in this article are those of the authors
and do not reflect the official policy or position of the
Department of the Navy, Department of Defense, or the
United States Government.


n

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REFERENCES

1. US Navy Dive Manual Revision 6. 2011 Oct;

(Change A):Section 20-2.3.
2. Cummins RO, Ornato JP, Thies WH, Pepe PE.
Improving survival from sudden cardiac arrest: the chain
of survival concept. Circulation 1991; 83: 1832-1847.

13. Ewy GA, Sanders AB. Alternative approach to improving

survival of patients with out-of-hospital primary cardiac
arrest. J Am Coll Cardiol. 2013 Jan 15; 61(2): 113-118.

3. Stiell I, et al. Advanced cardiac life support in out-ofhospital cardiac arrest. N Engl J Med 2004; 351:647-656.

14. Hardman JG, Wills JS, Aitkenhead AR. Factors determining the onset and course of hypoxaemia during apnea:
an investigation using physiological modelling. Anesth
Analg 2000; 90: 619-624.

4. Stiell I, Nichol G, Wells G, et al. Health-related quality

of life is better for cardiac arrest survivors who received
citizen cardiopulmonary resuscitation. Circulation 2003;
108: 1939-1944.

15. Noc M, Weil MH, Tang W, Turner T, Fukui M.

Mechanical ventilation may not be essential for initial
cardiopulmonary resuscitation. Chest 1995 Sep; 108(3):
821-827.

5. Rea TD, Eisenberg 5. MS, Culley LL, Becker L.

Dispatcher assisted cardiopulmonary resuscitation and
survival in cardiac arrest. Circulation 2001; 104: 2513-2516.

16. Turner I, Turner S, Armstrong V. Does the compression

to ventilation ratio affect the quality of CPR: a simulation
study. Resuscitation. 2002 Jan; 52(1): 55-62.
17. Cha KC, Kim YJ, Shin HJ, Cha YS, Kim H, Lee KH,
Kwon W, Hwang SO. Optimal position for external chest
compression during cardiopulmonary resuscitation: an analysis based on chest CT in patients resuscitated from cardiac
arrest. Emerg Med J. 2013 Aug; 30(8): 615-619.

6. Kindwall E, Whelan H. Hyperbaric medicine practice,

3rd Edition. 2008.
7. Rea TD, Fahrenbruch C, Culley L, et al. CPR with chest
compression alone or with rescue breathing. N Engl J Med
2010; 363: 423-433.
8. Ewy GA, Zuercher M, Hilwig RW, et al. Improved
neurological outcome with continuous chest compressions
compared with 30:2 compressions-to-ventilations cardiopulmonary resuscitation in a realistic swine model of out-ofhospital cardiac arrest. Circulation 2007; 116: 2525-2530.
9. Steen S, Liao Q, Pierre L, Paskevicius A, Sjberg T.
The critical importance of minimal delay between chest
compressions and subsequent defibrillation: a haemodynamic
explanation. Resuscitation. 2003 Sep; 58(3): 249-258.
10. Georgiou M, Papathanassoglou E, Xanthos T.
Systematic review of the mechanisms driving effective blood
flow during adult CPR. Resuscitation. 2014 Nov; 85(11):
1586-1593.
11. Turner I, Turner S, Armstrong V. Does the compression
to ventilation ratio affect the quality of CPR: a simulation
study. Resuscitation. 2002 Jan; 52(1):55-62.
12. Bobrow BJ, Ewy GA, Clark L, Chikani V, Berg RA,
Sanders AB, Vadeboncoeur TF, Hilwig RW, Kern KB.
Passive oxygen insufflation is superior to bag-valve-mask
ventilation for witnessed ventricular fibrillation out-ofhospital cardiac arrest. Ann Emerg Med. 2009 Nov; 54(5):
656-662.

Wright KT, Praske SP, Bhatt NA, et al.

18. Fodden DI, Crosby AC, Channer KS. Doppler

measurement of cardiac output during cardiopulmonary resuscitation. J Accid Emerg Med. 1996 Nov; 13(6): 379-382.
19. Hagihara A, Hasegawa M, et al. Prehospital epinephrine
use and survival among patients with out-of-hospital cardiac
arrest. JAMA 2012; 307(11): 1161-1168.
20. Jacobs IG, Finn JC, et al. Effect of adrenaline on
survival in out-of-hospital cardiac arrest: A randomized
double-blind placebo-controlled trial. Resuscitation 2011;
82(9): 1138-1143.
21. Sigurdsson G, Yannopoulos D, McKnite SH, Lurie KG.
Cardiorespiratory interactions and blood flow generation
during cardiac arrest and other states of low blood flow.
Curr Opin Crit Care. 2003 Jun; 9(3): 183-188.
22. Kot J. Controversies in hyperbaric medicine - Medical
devices and procedures in the hyperbaric chamber. Diving
Hyperb Med 2014; 44:223-227.
23. Callans D. Out-of-hospital arrest The solution is
shocking. N Engl J Med 2004; 351: 632-634.
24. Becker LB, Ostrander MP, Barrett J, Kondos GT.
Outcome of CPR in a large metropolitan area where are
the survivors? Ann Emerg Med 1991; 20:355-361.

77

UHM 2016, Vol. 43, No. 1 CARDIAC ARREST IN THE HYPERBARIC ENVIRONMENT: CASE REPORTS
25. Wang CH, Chang WT, Huang CH, Tsai MS, Yu PH,
Wang AY, Chen NC, Chen WJ. The effect of hyperoxia on
survival following adult cardiac arrest: a systematic review
and meta-analysis of observational studies. Resuscitation.
2014 Sep; 85(9): 1142-1148.
26. Eisenberg MS, Bergner L, Hallstrom A. Cardiac r
esuscitation in the community: importance of rapid provision
and implications for program planning. JAMA 1979; 241:
1905-1907.

28. Fullerton JN. Oxygen in resuscitation: a game of two

halves. Resuscitation. 2013 Jun; 84(6): 715-717.
29. Koster RW, Baubin MA, Bossaert LL, Caballero A,
Cassan P, Castrn M, Granja C, Handley AJ, Monsieurs KG,
Perkins GD, Raffay V, Sandroni C. European Resuscitation
Council Guidelines for Resuscitation 2010 Section 2.
Adult basic life support and use of automated external defibrillators. Resuscitation. 2010 Oct; 81(10): 1277-1292.

27. Spindelboeck W, Schindler O, Moser A, Hausler F,

Wallner S, Strasser C, Haas J, Gemes G, Prause G.
Increasing arterial oxygen partial pressure during cardiopulmonary resuscitation is associated with improved rates of
hospital admission. Resuscitation. 2013 Jun; 84(6):
770-775.

78

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