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(REBOA), has recently been popularized as a method of controlling noncompress-
ible bleeding in hemorrhagic shock.
During cardiac arrest, preclinical literature demonstrates that the occlusion
blood ow to the distal aorta effectively redirects the patient’s blood supply
toward the heart and the brain, helping to preserve their function [4]. Increased
ow improves coronary and cerebral perfusion and oxygenation. A signicant
body of preclinical evidence dating back to the early 1980s supports the balloon
occlusion of the aorta during NTCA as an adjunct to improve traditional advanced
cardiac life support (ACLS); however, human trials have been limited to case
series [5]. Recent advances in percutaneous balloon technology have broadened
this technique’s feasibility and set the stage for promising research into its role as
an adjunct to ACLS (Fig.10.1).
Fig. 10.1 Thoracic aortic balloon occlusion during cardiac arrest
J. Daley and J. Morrison
137
10.2 Nontraumatic Cardiac Arrest
10.2.1 Epidemiology
While many patients who experience cardiac arrest are elderly with signicant
comorbidities, a large proportion of victims of NTCA are younger, relatively healthy,
and could potentially survive their arrest with a meaningful quality of life. The mean
age of arrest has been reported to range from 72 to 78years old [6–8], while 33% of
patients in NTCA are of working age (18–64years old) [6]. A signicant number of
patients presenting in NTCA have a potentially reversible etiology of their arrest,
while rates of associated terminal illness among victims of NTCA have been reported
to be as low as 9.4% [7, 8]. A reversible etiology of cardiac arrest is dened as any
cause of arrest that if rapidly and effectively treated may allow the patient to recover
with signicant quality of life. Examples include myocardial infarction, pulmonary
embolism, hyperkalemia, and toxicological overdose.
Between 65% and 89% of NTCA have been estimated to be of primary cardiac
origin with coronary artery disease as the leading cause of arrest [9]. One study
estimated that 43% of arrests were due to acute myocardial infarction and 2% from
pulmonary embolism [10]. Another study found that on postmortem examination,
approximately 50% of patients had an obstructive coronary lesion that was the
likely cause of their arrest [9]. Between 6% and 15% of cases are estimated to have
a toxicological cause such as medication or illicit drug overdose [10, 11].
Historical information which can be obtained on patient arrival from the emer-
gency medical system (EMS) providers can be of signicant prognostic utility.
Patients who survive with good neurologic function typically have at least one of
the following signicant positive predictors: initial rhythm of ventricular brillation
or tachycardia, debrillation attempted prior to arrival to the emergency depart-
ment, early time to debrillation, witnessed arrest, and/or received bystander CPR
[9]. Physiologic data such as end tidal carbon dioxide (ETCO2) can also be of prog-
nostic utility. Patients who have ETCO2 values greater than 10mmHg have a sig-
nicantly higher likelihood of return of spontaneous circulation (ROSC) and
survival with good neurologic function [12].
10.2.2 Physiology
In the moments following a ventricular brillation arrest, blood ow throughout the
body continues after cardiac activity has ceased. Over a period of several minutes,
the pressure gradient between the aorta and the right atrium gradually equalizes
[13]. These reductions in ow to vital organs cause cerebral and coronary perfusion
pressures to plummet, hampering oxygen delivery and cardiac recovery.
Coronary perfusion pressure represents the gradient that drives blood ow
through capillary beds that perfuse the myocardium. It is calculated by subtracting
10 REBOA inNontraumatic Cardiac Arrest
138
the right atrial pressure from the diastolic aortic pressure, as the contracting heart
prevents coronary perfusion during systole [14]. Coronary perfusion pressure and
coronary artery ow are signicant predictors of increased rates of ROSC and sur-
vival to hospital discharge [12–15]. In a landmark study of 100 cardiac arrest
patients, Paradis etal. described a strong association between ROSC and a coronary
perfusion pressure greater than 15 mmHg [14]. Increases in coronary perfusion
pressure during a cardiac arrest are followed by improvements in cerebral perfusion
pressure and enhanced cerebral oxygenation [16].
Traditional ACLS is often unable to maintain the circulatory support required for
ROSC and preservation of neurologic function. During chest compressions, coronary
perfusion pressure rises gradually over minutes and falls abruptly when CPR is inter-
rupted, often becoming negative and impeding blood ow to the heart [17]. During
NTCA, ACLS generates coronary perfusion pressures between 0% and 30% of nor-
mal values, which are associated with a low probability of ROSC and survival [18,
19]. Even when compressing to a depth of 6.25cm, traditional CPR could only main-
tain 50% of prearrest coronary perfusion pressures in anesthetized pigs [20]. Coronary
perfusion pressures achieved with ACLS are rarely enough to attain adequate levels of
cerebral ow and oxygenation [16, 21], impeding neurologic recovery after ROSC.
While coronary perfusion pressure is critical to restoring cardiac activity, cere-
bral perfusion pressure is similarly important for neurologic preservation and recov-
ery. Cerebral perfusion pressure refers to the gradient between the carotid artery and
intra-cranial pressure, which drives cerebral blood ow and oxygen delivery to the
brain. Increases in ow through the carotid arteries serve to bolster the cerebral
perfusion pressure, increasing cerebral ow. Increased cerebral perfusion pressure,
cerebral ow, and carotid ow are associated with improved neurologic outcomes
in NTCA [12, 13, 22, 23].
Another more indirect marker of cardiac output and perfusion during NTCA is end
tidal carbon dioxide, a measure of the partial pressure of carbon dioxide at the end of
an exhalation. Its three main determinants are pulmonary ventilation, pulmonary per-
fusion (i.e., cardiac output), and cellular metabolism. During a cardiac arrest, pulmo-
nary perfusion is the predominant factor driving any uctuations and directly correlates
with cardiac output [12]. Levels greater than 10mmHg have been shown to be signi-
cantly associated with ROSC and can be trended to monitor CPR quality [12]. While
end tidal carbon dioxide is of clear clinical utility during cardiac arrest, its sensitivity
for ROSC has been reported to be between 70% and 90% and hence should not be
used as the sole determinant of prognostication during resuscitation [12].
10.3 Evidence fortheUse ofAortic Occlusion
inNontraumatic Cardiac Arrest
10.3.1 Preclinical Studies
Preclinical studies that examine the effectiveness of aortic occlusion use a ventricu-
lar brillation animal model of NTCA.Typically, the animal is placed under general
anesthesia, followed by the induction of ventricular brillation using an electric
J. Daley and J. Morrison
139
current. The animal is then left pulseless without intervention to simulate a period
of time that a person might lie unattended without bystander CPR. Investigators
then initiate either standard ACLS or ACLS with aortic balloon occlusion. Studies
can be broadly divided into several categories based on the duration of aortic occlu-
sion and whether a separate control group was utilized. Some studies involve inter-
mittent aortic occlusion using short periods of balloon ination and deation, while
others make use of continuous aortic occlusion. Additionally, many studies are of a
crossover design, comparing the hemodynamic effect of aortic balloon ination and
deation in the same animal and do utilize a separate control group. Other studies
focus on outcomes such as ROSC and neurologic function and compare these out-
comes in an experimental aortic occlusion group to a control group that received a
standard resuscitation.
10.3.1.1 Intermittent Occlusion
Six preclinical studies have tested the effectiveness of intermittent aortic occlusion
in animal models of ventricular brillation cardiac arrest [24–29]. The duration of
aortic occlusion ranged from brief ination during diastole (with systolic deation)
using IABPs to alternating periods of full aortic occlusion for up to 5min.
Two crossover studies examined the use of IABPs that inate during diastole and
deate with systole in a canine model. Authors found that during periods of IABP
support (compared to when the IABP was switched-off), animals had signicant
increases in coronary blood ow [24]. One study noted a near doubling of coronary
perfusion pressure as well as increased ETCO2, although no increase in systolic
blood pressure [26]. This suggests that while IABP support may assist with increas-
ing coronary perfusion, its effects on cerebral perfusion may be more limited.
Sesma etal. describe a crossover study where canines received two 5min periods
of aortic occlusion, interspersed by 5min periods of traditional ACLS without aor-
tic occlusion [29]. They noted improvements in hemodynamics during each period
of aortic occlusion that were reversed with aortic balloon deation. Coronary perfu-
sion pressure increased from 10.2 to 29.0mmHg in the initial period of aortic occlu-
sion, while ETCO2 underwent a more modest (yet statistically signicant) increase
from 19.2 to 26.1mmHg. The effects on coronary perfusion pressure and ETCO2
were similar for the second period of balloon ination.
Tang et al. describe the only controlled experiment using intermittent aortic
occlusion. Animals underwent 45s of aortic occlusion 5cm distal to the aortic valve
(preventing blood ow to the brain) every 2min and were compared to animals that
received a standard resuscitation without aortic occlusion. Each period of balloon
ination demonstrated increases in coronary perfusion pressure from a baseline of
approximately 10–50mmHg. This increase is of greater magnitude than that seen in
prior experiments, suggesting that the closer the balloon is placed to the heart, the
greater the increase in cardiac perfusion. This increase in coronary perfusion led to
a signicant improvement in 48-h survival. All ten animals that underwent intermit-
tent aortic occlusion remained alive at 48h. Perhaps more impressive is that all of
these animals had near-normal neurologic function, despite periods of 45s during
aortic balloon ination where their brain did not receive blood ow. In comparison,
only one animal out of ten survived to 48h in the control group.
10 REBOA inNontraumatic Cardiac Arrest
140
10.3.1.2 Continuous Occlusion
Nine studies of continuous balloon occlusion in animal models of NTCA have
shown meaningful increases in hemodynamic outcomes or mortality [30–38], while
one study failed to do so [39]. Several research groups investigated the effects of
aortic occlusion on cardiac and cerebral perfusion using a crossover study design,
where animals underwent both a period of balloon ination and a period of standard
resuscitation without balloon ination. Gedeborg et al. demonstrated an 86%
increase in coronary artery blood ow and a 33% decrease in cardiac output during
periods of aortic occlusion [34]. The noted reduction in cardiac output is likely due
to increased afterload caused by balloon ination. In a similar study, Spence etal.
reported increases in coronary and cerebral blood ow of approximately 100% dur-
ing periods of aortic occlusion [31]. These results suggest that aortic occlusion is
not only effective at increasing cardiac perfusion, but may have benecial effects on
cerebral perfusion as well. Gedeborg etal. reported similar ndings, noting that
carotid artery blood ow (a surrogate for cerebral blood ow) increased by 63%
during periods of aortic occlusion.
Controlled preclinical studies of aortic occlusion note similar effects on hemody-
namics, as well as signicantly higher rates of ROSC and short-term survival with
good neurologic status. Investigators found that groups treated with aortic occlusion
had higher mean arterial pressures [34], increased cerebral perfusion [36–38], and
improved coronary perfusion [33, 37], when compared to control animals receiving
standard ACLS. Gedeborg et al. reported that mean arterial pressure (MAP) in
experimental animals was 68mmHg after ination of the aortic balloon, compared
to 48mmHg in control animals that received a sham-balloon. In a similar experi-
ment, Rubertsson et al. noted coronary perfusion pressure of approximately
25mmHg in the aortic occlusion group, compared to that of only 10mmHg in the
control group.
Importantly, improvements in the hemodynamics of experimental aortic occlu-
sion animals resulted in increased rates of ROSC as well as short term survival. In
one study in swine with an 8min simulated down-time where no CPR was per-
formed, 9 out of 13 (69%) aortic balloon animals had ROSC compared to only 3 out
of 13 (23%) animals from the control group [34]. A similarly conducted study noted
a signicant improvement in the rate of ROSC in aortic balloon animals. After
10min of ventricular brillation without CPR, followed by either traditional ACLS
or ACLS with aortic occlusion, 7 out of 8 (87%) experimental animals compared to
3 of 10 (30%) control animals achieved ROSC. There was a trend toward greater
24-h survival with 5 of 8 (63%) experimental animals surviving compared to 3 of 10
(30%) controls [33].
While the literature is replete with studies documenting the benecial effects of
aortic occlusion on hemodynamics and survival, there is one study that goes against
this trend. In 2002, Liu etal. conducted an experiment where swine were subjected
to ventricular brillation. After 8min without any resuscitative efforts, the experi-
mental group received balloon occlusion combined with an intravenous infusion of
normal saline, while the control group only received sham balloon occlusion.
Investigators found no difference in coronary perfusion pressure, rates of ROSC (6
J. Daley and J. Morrison
141
out of 10in experimental group, 7 out of 10in control group), or 24-h survival. It is
unclear why this experiment failed to replicate the results of those previously dis-
cussed. It is possible that by infusing normal saline in the experimental animals,
investigators increased their right atrial pressure, in effect reducing their coronary
perfusion pressure to the level of control animals. As there was no difference in
coronary perfusion pressures, it is not surprising that rates of ROSC and survival
remained similar between the two groups.
Several studies examined the use of the intra-aortic infusion of vasopressors and
demonstrated positive effects on cardiac output, however, no effect on cerebral per-
fusion. Intra-aortic vasopressin and balloon occlusion was associated with an
increase in coronary perfusion pressure during CPR in swine, but had no effect on
cerebral cortical blood ow [37]. In a similar study by the same authors, the admin-
istration of intra-aortic epinephrine had no signicant effect on cerebral cortical
blood ow and possibly had an adverse effect, likely due to the vasoconstrictive
effects of epinephrine [40]. A study by a different group found no difference in
coronary perfusion pressure, rates of ROSC, or survival, when animals were given
intra-aortic epinephrine. However, they did nd that experimental animals had
much higher rates of hemorrhagic myocardial necrosis on autopsy, suggesting that
intra-aortic epinephrine may have a cardiotoxic effect.
10.3.1.3 Selective Aortic Arch Perfusion
Certain aortic balloon catheters are capable of infusing large volumes of various
substances, such as hyper-oxygenated compounds and medications, directly proxi-
mal to the site of aortic balloon occlusion, a technique known as selective aortic
arch perfusion (SAAP). Pioneers of SAAP believe that it may provide superior
improvements in coronary and cerebral perfusion as compared to balloon occlusion
alone. By delivering a high-volume infusion directly into the aortic arch, aortic
pressures might increase further and bolster coronary perfusion pressure. Infusions
with supra-normal levels of oxygen may provide additional benets, such as
increased oxygen delivery to the myocardium and brain. SAAP is a technique that
is still under preclinical development and has not yet been tested in humans.
A study of cardiac arrest in canines with a prolonged no-compression down time
(20min) who received an infusion of stroma-free ultra-puried bovine hemoglobin
in combination with aortic occlusion demonstrated signicant differences in coro-
nary perfusion pressures and survival. Animals that underwent aortic occlusion with
a puried hemoglobin infusion had a mean coronary perfusion pressure of 62mmHg
and a 70% survival rate, compared to coronary perfusion pressure of 33mmHg and
survival rate of only 20% in those that underwent standard ACLS alone [41]. In a
similar trial, the same authors demonstrated a dose–response relationship between
increasing concentrations of the puried hemoglobin infusion and survival [42]. A
separate research group investigated the use of aortic occlusion and infusion of an
oxygen-carrying uorocarbon emulsion and found similar effects on coronary perfu-
sion pressure and survival in the SAAP animals [43, 44]. While SAAP may be more
effective than aortic occlusion alone, it requires a much larger catheter (12Fr vs. 7Fr)
than aortic occlusion alone, which increases the risk of extremity complications.
10 REBOA inNontraumatic Cardiac Arrest
142
10.3.2 Clinical Evidence
The extent of the literature involving human subjects and aortic balloon support
during NTCA is limited to several case reports and case series, three of which are
from the 1980s [45–49]. The advent of the rst percutaneous intra-aortic balloon
pump in the late 1970s made it possible to utilize aortic balloon technology in car-
diac arrest patients. Bregman et al. provided the rst published account of this,
describing the placement of IABPs in three patients undergoing cardiac arrest. All
of the patients died, although they did not provide details of the circumstances of the
patients’ cardiac arrest [45]. Subsequently, Philips etal. reported on ve patients
that underwent IABP placement during cardiac arrest [46]. All were initially in
asystole and one patient survived until hospital discharge; no complications of bal-
loon insertion were reported.
Gottlieb etal. built upon their work when, in 1986, they describe using a modi-
ed ambulance to place IABPs outside of the hospital in three cardiac arrest patients
[47]. Two patients, initially in a pulseless electrical activity rhythm, had ROSC and
were subsequently discharged from the hospital with good neurologic function. The
third suffered cardiac arrest from an ST-elevation myocardial infarction (STEMI).
This patient achieved ROSC and notably, their ST-elevations improved or disap-
peared during periods of IABP support, suggesting a clinically signicant increase
in cardiac perfusion. Unfortunately, and likely due to their prolonged resuscitation
prior to IABP placement, the patient had a poor neurologic outcome. Deakin etal.
similarly described a report of two patients in cardiogenic shock, already dependent
on IABPs, who had a cardiac arrest with their IABP in place [48]. In each, the aortic
balloon was continuously inated during their cardiac arrest and authors noted mild
increases in coronary perfusion pressure (10 and 2mmHg, respectively) after bal-
loon ination; however, both patients died. It is unlikely that these patients would
have survived regardless of their treatment as their cardiac function was extremely
poor even before their cardiac arrest.
The most compelling case report for the use of aortic occlusion in NTCA comes
from Aslanger etal. in 2009 [49]. A 74-year-old female presented to the emergency
department with a myocardial infarction and was taken to the cardiac catheteriza-
tion laboratory. She was found to have a 95% stenotic lesion of her mid left circum-
ex coronary artery but due to vessel tortuosity, the interventionalist was unable to
place a stent for revascularization. She was transferred to the cardiac care unit where
her hemodynamics quickly decompensated. Investigators initiated a dopamine infu-
sion, but the patient sustained a pulseless electrical activity (PEA) cardiac arrest that
devolved into asystole soon after. After 25min of ACLS, authors placed an over-
sized intra-aortic balloon pump and used it to continuously occlude the aorta. The
authors noted that 45s after balloon occlusion, the patient began to spontaneously
gasp and had ROSC, with a normal sinus rhythm established after 1min. She was
placed on IABP support and eventually discharged from the hospital and had made
a “good recovery” at a 3months follow-up visit. It is unlikely that she would have
had ROSC without the aortic balloon ination, as patients who receive ACLS for
greater than 20min without ROSC have an extremely low probability of ROSC with
J. Daley and J. Morrison
143
continued resuscitation [50, 51]. Furthermore, the temporal association between
aortic balloon ination followed by ROSC less than 1min later suggests that it
played a signicant role in her successful resuscitation.
10.3.3 Feasibility ofREBOA inNontraumatic Cardiac Arrest
Femoral artery cannulation and aortic balloon placement during NTCA in the pre-
hospital and hospital environment are technically feasible. The most difcult aspect
of the REBOA procedure is obtaining femoral artery access, especially when
patients are undergoing chest compressions [52]. The use of bedside ultrasound
improves femoral artery cannulation success while allowing real-time conrmation
of the location of the aortic catheter tip [3, 53]. The success of emergency depart-
ment and prehospital extra corporeal membranous oxygenation (ECMO) programs
further support the practicality of this concept, as these teams routinely place large
femoral arterial catheters in patients undergoing ACLS for cardiac arrest [54–56].
There are an increasing number of centers in the United States and Europe who can-
nulate cardiac arrest patients for veno-arterial ECMO (often termed “E-CPR”) [57].
Additionally, there are several case series that report the placement of IABPs in
patients undergoing chest compressions [45–47], while the surgical literature con-
tains many examples of REBOA use in patients in traumatic cardiac arrest [3, 58–
60]. Manning etal. further demonstrated the feasibility of blind femoral arterial and
venous cannulation and aortic catheter placement in 22 victims of NTCA in the
prehospital environment. They utilized these catheters to measure coronary perfu-
sion pressure in real-time to improve the delivery of CPR quality.
Conclusion: Implementation ofREBOA forNontraumatic Cardiac Arrest
Patients who undergo prolonged resuscitation without resumption of sustained
cardiac activity have an extremely poor prognosis and can be considered to have
failed traditional ACLS; however, these patients may still be neurologically via-
ble [51]. In a study of 1204 cases of NTCA, 90% of those who achieved ROSC
had done so by 24min of CPR, with rates of ROSC declining signicantly after
that point. Further research shows that after 21min of conventional ACLS in
patients without ROSC, the probability of neurologically intact survival drops
precipitously [6, 51, 61]. It is highly unlikely that patients without ROSC will
survive their arrest with good neurologic outcome once traditional resuscitation
has exceeded 21 min. Based on the compelling animal data and human case
series, it is conceivable that these patients may still benet from REBOA.
To maximize the probability of a patient’s return to a good quality of life,
detailed inclusion criteria must be applied before utilizing REBOA during a car-
diac arrest. REBOA should only be considered if the physician believes that the
patient has a reversible etiology of their arrest that may be immediately treated. For
example, in a patient with acute myocardial infarction who is otherwise healthy,
REBOA may be able to provide enough circulatory support to bridge the patient to
denitive therapy, such as the cardiac catheterization laboratory or ECMO.
10 REBOA inNontraumatic Cardiac Arrest
144
Physicians at the bedside must assess for contraindications, such as presence
of an end-stage terminal illness, severe neurologic impairment at baseline, or
suspected devastating neurologic injury as the etiology of arrest. Before initia-
tion of REBOA, the patient must have failed therapy with traditional ACLS; a
requirement that the authors consider satised after 20min of resuscitation with
ACLS and no ROSC.Finally, the ideal patient should show at least some signs
of life prior to the initiation of REBOA, which may include ndings such as
reactive pupils, agonal breathing, end tidal carbon dioxide greater than 10mmHg,
arterial relaxation pressure greater than 17mmHg, any cardiac activity on bed-
side echocardiogram, or a shockable rhythm.
While evidence for the use of aortic occlusion in NTCA in animal models is
promising, experience in humans is too limited to advocate for immediate imple-
mentation of this technique outside of a research setting. What is clear is that
REBOA in NTCA deserves future study on a larger scale to determine if it may
be effective in humans. The selective perfusion of the heart and brain to augment
traditional ACLS through aortic occlusion makes sense physiologically, as the
laws of uid dynamics dictate that when the same blood volume moves through
a reduced vascular bed, the pressure will increase. The concept is supported by
decades of preclinical research and has been shown to be feasible in humans. It
is apparent that alternative therapies are required if we intend to signicantly
advance our ability to provide resuscitative care to patients in cardiac arrest. The
use of REBOA as an adjunct to ACLS is an innovative strategy and is deserving
of further consideration and rigorous clinical investigation.
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10 REBOA inNontraumatic Cardiac Arrest