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11 • Resuscitative Endovascular Balloon Occlusion of the Aorta 135
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injury, as well as neurologic compromise. Moreover, the
release of inammatory mediators from this process com-
due to hyperperfusion such as cerebral edema, intracranial
hemorrhage, and myocardial dysfunction.
Future Advances
As we strive to achieve zero preventable deaths from uncontrolled hemorrhage, the ability to establish aortic occlusion for resuscitation both efciently and safely is critical.
Though not novel, the utilization of an endovascular balloon for aortic occlusion in trauma is a recent phenomenon
with increasing popularity as the technology improves and
practitioners become more familiar with the technique.
Future directions for REBOA include evolution of its technique to prolong physiologically tolerable occlusion times
such as via variable aortic occlusion methods and adjunct
procedures to minimize reperfusion injury. The successful
application of REBOA for traumatic noncompressible torso
hemorrhage has led to its consideration in other clinical scenarios of hemorrhagic shock as well. Ongoing controversies such as its use in patients undergoing cardiopulmonary
resuscitation as well as in patients with nontruncal injuries
should continue to be examined as increasing clinical data
becomes available.
References
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22. Morrison JJ, Ross JD, Markov NP. The inammatory sequelae of aor-
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25. Seamon MJ, Haut ER, Van Arendonk K, et al. An evidence-based
approach to patient selection for emergency department thoracotomy:
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26. Moore HB, Moore EE, Burlew CC, etal. Establishing benchmarks for
resuscitation of traumatic circulatory arrest: success-to-rescue and
survival among 1,708 patients. J Am Coll Surg. 2016;223:42–51.
27. Inoue J, Shiraishi A, Yoshiyuki A, Haruta K, Matsui H, Otomo Y.
Resuscitative endovascular balloon occlusion of the aorta might be
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analysis. J Trauma Acute Care Surg. 2016;80:559–567.
28. Abe T, Uchida M, Nagata I, Saitoh D, Tamiya N. Resuscitative endo-
vascular balloon occlusion of the aorta versus cross clamping among
patients with critical trauma: a nationwide cohort study in Japan. Crit
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29. DuBose JJ, Scalea TM, Brenner M, etal. The AAST prospective Aor-
tic Occlusion for Resuscitation in Trauma and Acute Care Surgery
(AORTA) registry: data on contemporary utilization and outcomes
of aortic occlusion and resuscitative balloon occlusion of the aorta
(REBOA). J Trauma Acute Care Surg. 2016;81:409–419.
30. Brenner M, Inaba K, Aiol A, etal. Resuscitative endovascular bal-
loon occlusion of the aorta and resuscitative thoracotomy in select
Association for the Surgery of Trauma’s Aortic Occlusion in Resuscitation for Trauma and Acute Care Surgery registry. J Am Coll Surg.
2018;226:730–740.
31. Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE, Elia-
son JL. A systematic review of the use of resuscitative endovascular
balloon occlusion of the aorta in the management of hemorrhagic
shock. J Trauma Acute Care Surg. 2016;80:324–334.
32. Romagnoli A, Teeter W, Pasley J, etal. Time to aortic occlusion: it’s all
about access. J Trauma Acute Care Surg. 2017;83:1161–1164.
33. UK-REBOA Trial. https://W3.Abdn.Ac.Uk/Hsru/REBOA/Public/Pub-
lic/Index.Cshtml. Accessed October 14, 2019.
34. Stannard A, Eliason JL, Rasmussen TE. Resuscitative endovascular
balloon occlusion of the aorta (REBOA) as an adjunct for hemorrhagic shock. J Trauma. 2011;71:1869–1872.
35. Kalish J, Eslami M, Gillespie D, etal. Routine use of ultrasound guidance
in femoral arterial access for peripheral vascular intervention
decreases groin hematoma rates. J Vasc Surg. 2015;61:1231–1238.
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36. Bogert JN, Patel BM, Johnson DJ. Ultrasound optimization for resus-
citative endovascular balloon occlusion of the aorta. J Trauma Acute
Care Surg. 2017;82:204–207.
37. Scott DJ, Eliason JL, Villamaria C, etal. A novel uoroscopy-free, resus-
citative endovascular aortic balloon occlusion system in a model of
hemorrhagic shock. J Trauma Acute Care Surg. 2013;75:122–128.
38. Pezy P, Flaris AN, Prat NJ, et al. Fixed-distance model for balloon
placement during uoroscopy-free resuscitative endovascular balloon occlusion of the aorta in a civilian population. JAMA Surg.
2017;152:351–358.
39. Eliason JL, Derstine BA, Horbal SR, et al. CT correlation of skeletal
landmarks and vascular anatomy in civilian adult trauma patients:
implications for resuscitative endovascular balloon occlusion of the
aorta (REBOA). J Trauma Acute Care Surg. 2019;87:S137–S145.
40. Stannard A, Morrison JJ, Sharon DJ, Eliason JL, Rasmussen TE.
Morphometric analysis of torso arterial anatomy with implications for resuscitative aortic occlusion. J Trauma Acute Care Surg.
2013;75:S169–S172.
41. Kim DH, Chang SW, Matsumoto J. The utilization of resuscitative
endovascular balloon occlusion of the aorta: preparation, technique,
and the implementation of a novel approach to stabilizing hemorrhage. J Thoracic Dis. 2018;10:5550–5559.
42. Moore HB, Moore EE, Liras IN, et al. Targeting resuscitation to
normalization of coagulating status: hyper and hypocoagulability
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43. Moore EE, Knudson MM, Burlew CC, etal. Dening the limits of resus-
citative emergency department thoracotomy: a contemporary Western Trauma Association perspective. J Trauma. 2011;70:334–339.
44. Burlew CC, Moore EE, Stahel PF, et al. Preperitoneal pelvic packing
reduces mortality in patients with life-threatening hemorrhage due to
unstable pelvic fractures. J Trauma Acute Care Surg. 2017;82:233–242.
45. Adnan SM, Wasicek PJ, Crawford A, et al. Endovascular control of
pelvic hemorrhage: concomitant use of resuscitative endovascular
balloon occlusion of the aorta and endovascular intervention. J
Trauma Acute Care Surg. 2019;86:155–159.
46. Ogura T, Lefor AT, Nakano M, Izawa Y, Morita H. Nonoperative man-
agement of hemodynamically unstable abdominal trauma patients
with angioembolization and resuscitative endovascular balloon occlusion of the aorta. J Trauma Acute Care Surg. 2015;78:132–135.
47. DuBose JJ. How I do it: partial resuscitative endovascular balloon
occlusion of the aorta (P-REBOA). J Trauma Acute Care Surg.
2017;83:197–199.
48. Williams TK, Neff LP, Johnson MA, etal. Automated variable aortic
control versus complete aortic occlusion in a swine model of hemorrhage. J Trauma Acute Care Surg. 2017;82:694–703.
49. Kuckelman JP, Barron M, Moe D, et al. Extending the golden hour
for zone 1 resuscitative endovascular balloon occlusion of the aorta:
improved survival and reperfusion injury with intermittent versus
continuous resuscitative endovascular balloon occlusion of the aorta
in a porcine severe truncal hemorrhage model. J Trauma Acute Care
Surg. 2018;85:318–326.
50. Simon MA, Tibbits EM, Hoareau GL, et al. Lower extremity cooling
reduces ischemia-reperfusion injury following zone 3 REBOA in a porcine hemorrhage model. J Trauma Acute Care Surg. 2018;85:512–518.
51. Williams AM, Bhatti UF, Dennahy IS, etal. Traumatic brain injury
may worsen clinical outcomes after prolonged partial resuscitative
endovascular balloon occlusion of the aorta in severe hemorrhagic
shock model. J Trauma Acute Care Surg. 2019;86:415–423.
52. Ordoñez CA, Manzano-Nunez R, Parra MW, etal. Prophylactic use of
resuscitative endovascular balloon occlusion of the aorta in women
with abnormal placentation: a systematic review, meta-analysis, and
case series. J Trauma Acute Care Surg. 2018;84:809–818.
53. Reynolds CL, Celio AC, Bridges LC, etal. REBOA for the IVC? Resuscita-
tive balloon occlusion of the inferior vena cava (IVC) to abate massive
hemorrhage in retrohepatic cava injuries. J Trauma Acute Care Surg.
2017;83:1041–1046.
54. Kelm M, Perings SM, Jax T, etal. Incidence and clinical outcome of
iatrogenic femoral arteriovenous stulas: implications for risk stratication and treatment. J Am Coll Cardiol. 2002;40:291–297.
55. Brenner ML, Moore L, Teeter W, et al. Exclusive clinical experience
with a lower prole device for resuscitative endovascular balloon
occlusion of the aorta (REBOA). Am J Surg. 2019;217:1126–1129.
56. Matsumura Y, Matsumoto J, Kondo H, etal. Fewer REBOA complica-
tions with smaller devices and partial occlusion: evidence from a multicentre registry in Japan. Emerg Med J. 2017;34:793–799.
57. Teeter WA, Matsumoto J, Idoguchi K, etal. Smaller introducer sheaths
for REBOA may be associated with fewer complications. J Trauma
Acute Care Surg. 2016;81:1039–1045.
58. Saito N, Matsumoto H, Yagi T, etal. Evaluation of the safety and fea-
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59. Davidson AJ, Russo RM, Reva VA, etal. The pitfalls of resuscitative
endovascular balloon occlusion of the aorta: risk factors and mitigation strategies. J Trauma Acute Care Surg. 2018;84:192–202.
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Endovascular Variable
Aortic Control
MICHAELA GAFFLEY and TIMOTHY K. WILLIAMS
Introduction
Resuscitative endovascular balloon occlusion of the aorta
(REBOA) is increasingly utilized for patients with exsanguinating truncal hemorrhage.1 This treatment has
proven effective at rapidly restoring perfusion to the heart
and brain, while simultaneously minimizing hemorrhage
below the level of occlusion. However, this intervention
is encumbered by the progressive ischemic burden that
begins at the moment of balloon occlusion.2 To address
these issues, partial ow strategies have been developed
and tested in applied research models and are increasingly
being utilized in the care of patients. To date, these partial
ow modalities have been performed manually, which represents a signicant limitation to widespread adoption.3
These limitations include the demand for continuous
monitoring of the balloon and the difculty in maintaining a stable degree of partial aortic ow. To address some
of the fundamental limitations surrounding real-world
implementation of these partial ow strategies, the concept of endovascular variable aortic control (EVAC) has
been developed.4 EVAC is an automated technology that
controls aortic ow by precisely regulating ination and
deation of a balloon catheter. As it applies to hemorrhage control, EVAC can specically be used to achieve a
low- volume distal aortic ow to strike a delicate balance
between ongoing hemorrhage and progressive ischemic
injury, a therapeutic modality we have termed regional
perfusion optimization (REPO).
5
The Problems With REBOA
REBOA prolongs survival prior to denitive surgical hemostasis by decreasing distal hemorrhage below the level
of occlusion and augmenting proximal perfusion to the
heart, lungs, and brain. However, the benets of REBOA
are quickly offset by progressive ischemia below the level
of occlusion (limiting its duration of use to 40 to 60 minutes; Fig. 12.1).6 Severe hypertension above the balloon
may be detrimental to patients with noncompressible torso
hemorrhage (NCTH) and concomitant traumatic brain
injuries. It has been reported that the mortality rate in
brain-injured patients requiring REBOA as a resuscitative
adjunct approaches 50%,6 with case reports demonstrating
increased intracranial hemorrhage volumes after brief periods of REBOA. Physicians within the trauma community
have hypothesized that the supraphysiologic blood pressure
and carotid blood ow created by REBOA may account for
these early clinical ndings.
In addition, complete aortic occlusion with REBOA poses
challenges at the time of balloon deation, where abrupt
washout of ischemic metabolites during reperfusion can
produce life-threatening electrolyte abnormalities and
acid-base disturbances. Additionally, balloon deation may
result in profound hemodynamic instability, in part due to
the loss of distal vascular tone, which is compounded by the
ensuing ischemia reperfusion injury (Table 12.1).2 However, this currently remains the most expeditious manner
of managing NCTH, particularly in austere environments.
PARTIAL FLOW AS A STRATEGY TO ADDRESS
LIMITATIONS OF REBOA
To address these limitations of REBOA, partial REBOA
(pREBOA) has been proposed as an alternative to complete
occlusion, to avoid both hypotension and hypertension.
Additionally, this technique can minimize ischemic injury
to downstream organs by allowing some variable amount
of blood ow beyond the balloon. In principle, pREBOA
involves partial deation of the balloon catheter, typically
via means of manual syringe, thereby allowing some blood
ow beyond the balloon.7 Titration of the balloon can be
performed to target a blood pressure goal above or below
the balloon. To date, this procedure remains ill-dened and
is performed manually in the clinical setting, with no rm
consensus on how it should be implemented to ensure optimal outcomes.
Performing pREBOA has signicant limitations regardless of the methodology used. One principle limitation
stems from the inherent challenge of carefully titrating
aortic blood ow using a conventional aortic balloon
catheter. As an aortic balloon is deated from the state of
complete occlusion (no downstream ow), a steep inection point is reached where small changes in balloon lling
volume result in large changes in downstream aortic blood
ow.8 Additionally, the concurrent decrease in vascular
tone below the balloon induced by even brief periods (less
than 5 minutes) of complete aortic occlusion can result in
signicant decrease in the blood pressure above the balloon
during deation. This observation reects the fundamental
hemodynamic principle known as Poiseuille’s Law, where
ow is proportional to the radius of the vessel to the fourth
power. This exponential return of aortic blood ow therefore necessitates precise titration of balloon lling volume
to maintain stable ow rates. Even when balloon titration
is performed while already at a partial ow state, very small
balloon volume changes (less than 10 µL) can result in measurable change in aortic ow, highlighting the need for high
delity in this process.4 Achieving this level of delity with
137
138 SECTION 3 • Emerging Technologies and New Approaches to Vascular Trauma and Shock
Peak lactate
Lactate (mg/dL)
45 minu
60 minu
90 minu
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14
12
10
8
6
4
2
0
tes
Fig. 12.1 Resuscitative endovascular balloon occlusion of the aorta
results in progressive ischemic burden over time.
Table 12.1 Consequences of Prolonged Complete
Aortic Occlusion
Proximal Effects Distal Effects Systemic Effects
↑ Aortic afterload ↓ Cardiac preload Washout of toxic
↑ Blood pressure ↓ Blood pressure Altered vascular tone
↑ Blood flow ↓ Blood flow Hemodynamic instability
End organ
dysfunction
End organ
dysfunction
tes
tes
metabolites
Dysregulated immune
response
a manual syringe is challenging at best. Optimized balloon
designs may improve the deation prole during pREBOA
and allow for larger volume changes with lower degrees of
change in aortic ow; however, these devices have not made
it into clinical practice as of yet.
For these reasons, manual pREBOA requires a skilled end
user, which represents a signicant limitation to broader
adoption within the trauma community for users with
infrequent exposure to this technology. It is also not a practical solution in environments where providers represent a
scarce resource, as the constant need to attend to the balloon detracts from other vital aspects of patient care and
negates the possibility of simultaneously caring for multiple injured patients. Therefore, alternate approaches are
needed to enable extending the duration of REBOA-like
technologies.
EVAC Concept—Automated Partial
Aortic Flow Control
To overcome the limitations associated with manual pREBOA
being performed with a conventional compliant aortic occlusion balloon, our group developed the concept of EVAC. The
EVAC concept was initially developed to further rene our
management of NCTH in austere military environments,
where delayed transport or prolonged eld care is anticipated or required, enabling extended duration of intervention beyond what is survivable with sustained complete
aortic occlusion. Some of the same fundamental benets of
pREBOA can be targeted using the EVAC approach; however,
there are fundamental differences that differentiate the two
strategies. Most importantly is that EVAC represents an automated process to control aortic ow as opposed to the manual aortic ow control achieved with pREBOA. Conceptually,
EVAC can be envisioned as a spigot or valve, where ow can
be controlled across the full spectrum, from zero ow to full,
unimpeded ow. When applied to hemorrhage control, EVAC
can achieve very stable hemodynamics below the level of
ow restriction, thereby avoiding sudden and abrupt changes
in downstream blood ow that could result in clot destabilization and exacerbation of hemorrhage.
From our robust experience in performing manual pREBOA, frequent “titrations” are required to maintain a stable
degree of aortic ow, on the order of every few seconds to
several times a minute even during steady state conditions.
This frequency can be increased by other factors such as
medication administration, uid or blood administration,
or acute blood loss. By automating this process of balloon
titration, EVAC reduces the burden on the provider from
what can be a very time-intensive and task-focused intervention. This cognitive and procedural ofoading using
automation enables the provider to engage in higher level
aspects of direct patient care. Additionally, this capability is
appealing for resource-constrained environments because
it creates the potential for the provider to intensively support multiple patients simultaneously, thereby serving as a
force multiplier.
REGIONAL PERFUSION OPTIMIZATION
EVAC can be conceptualized as a technique to regulate aortic ow across the full spectrum, yet the therapeutic goals
of EVAC are dened by the context and methods of how this
technique is applied. With respect to hemorrhage control
and hemodynamic support for hypovolemic patients, our
group and others have postulated that delivering a stable,
low amount of aortic ow can be used to mitigate the effects
of sustained aortic occlusion.9 This conceptual therapy,
termed regional perfusion optimization (REPO), embodies
physiologic and hemodynamic effects both above and below
the level of occlusion, with preference given to the maintenance of low-volume ow to distal vascular beds. The
therapeutic goals of REPO are to (1) minimize tissue ischemia below the level of occlusion, (2) promote hemostasis
or minimize ongoing hemorrhage to prevent exsanguination, and (3) minimize adverse effects on proximal vascular
beds, specically severe hypertension and excessive cardiac
afterload. The aggregate effect of this therapy is to produce
less secondary injury, thereby minimizing the impact of the
intervention at the time of reperfusion. In doing so, REPO
seeks to minimize subsequent resuscitation requirements
and ideally improve survival. Additionally, REPO could be
applied prior to the threshold at which one would utilize
REBOA as a means of impacting the morbidity associated
with large-volume transfusions, vasopressors, and crystalloids that may be required in the context of higher levels of
hemorrhage and ischemic injury. We have found that utilizing the EVAC technique to achieve REPO results in signicant decreases in resuscitation requirements (Fig. 12.2).
REPO embodies a ow-based approach to resuscitation,
which is optimizing blood ow to downstream tissue beds
10
12 • Endovascular Variable Aortic Control 139
To tal resuscitation fluids
AB
To tal vasopressors
06
Lactate
Peak lactateFinal lactate
Lactate mg/dL
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based on the patient’s unique physiology. This represents
a departure from pressure-based resuscitation paradigms,
where blood pressure support or augmentation is the principle focus of the resuscitative effort. The REPO concept
makes the assumption that controlling and optimizing blood
ow within a vessel as opposed to blood pressure represents
a more valuable surrogate marker for tissue perfusion, the
sustainer of organ viability. By delivering a low level of distal
blood ow (approximately 10%–20% of native visceral and
lower extremity blood ow) to injured tissue beds, our group
and others have demonstrated that the ischemic burden of
aortic occlusion can be substantially mitigated (Fig. 12.3).11
Additionally, this approach has been shown to result in tolerable levels of hemorrhage in the context of severe liver
and major vascular injury. Taken together, these benecial
effects of REPO serve to extend the maximal duration of
intervention for REBOA well beyond what can be expected
from equivalent durations of complete aortic occlusion.
Although REPO represents a ow-based therapy, it is
important to emphasize that direct blood ow measurements are not currently easily obtained, making a owbased resuscitation challenging outside of experimental
models. Therefore, it becomes necessary to model ow from
900
8000
7000
6000
5000
4000
3000
Plasmalyte (mL)
2000
1000
0
Fig. 12.2 Resuscitation requirements: Regional perfusion optimization
(REPO) resulted in less than half the amount of (A) fluids and (B) vasopressors during automated critical care as compared to resuscitative
endovascular balloon occlusion of the aorta (REBOA).
12
10
8
6
4
2
0
Fig. 12.3 Ischemic burden: Regional perfusion optimization (REPO)
resulted in lower peak and final lactate levels than resuscitative endovascular balloon occlusion of the aorta (REBOA).
REBOA
REPO
0
50
40
30
20
Norepinephrine (ng/kg)
10
0
REBOA
REPO
REBOA
REPO
clinically available metrics, specically utilizing blood
pressure measurements. It is important to understand how
these two distinct hemodynamic values relate and extrinsic
factors that inuence this relationship. Under certain
conditions, blood pressure and ow correlate in a predictable
fashion; however, certain situations make this relationship
unpredictable and/or unreliable.
Various interventions inuence this relationship, including uid, blood, or medications. Additionally, it is important
to recognize that partial aortic occlusion creates unique
hemodynamic relationships not present in a healthy native
aorta. For instance, proximal blood pressure and distal
blood pressure tend to directly correlate with blood ow
during active volume administration or from volume loss,
in the absence of any aortic occlusion or in the presence
of a statically held balloon. However, administration of a
pure alpha agonist such as phenylephrine (with or without
a static balloon) will variably increase systemic vascular
resistance, thereby raising blood pressure, yet decreasing
blood ow. Active balloon titration results in yet a different
hemodynamic effect, producing an increase in proximal
blood pressure, a decrease in distal pressure, and a decrease
in aortic ow. Inversely, balloon deation tends to result in
a decrease in proximal blood pressure, and an increase in
both distal pressure and aortic ow.
Although general trends are predictable, meaningful
quantication of blood ow based on changes in blood
pressure due to these interventions is not feasible in most
instances. Nonetheless, our group has evaluated these
hemodynamic relationships in a rigorous fashion, revealing some clinically useful insights. We have found that
the aortic blood pressure below the balloon correlates in
a fairly linear fashion with blood ow beyond the balloon
at low-ow states (0%–40% of baseline aortic ow), over
an array of hemorrhage volumes (0%–40% total circulating blood volume) (Fig. 12.4).12 Such an approach can
be implemented clinically by rst measuring the pressure
below the occlusion balloon at full occlusion (by denition
a zero-ow state), then targeting a distal blood pressure of
approximately 7 to 10 mm Hg above the occlusion value,
which experimentally results in approximately 5% to 10%
of native distal aortic ow. It is important to emphasize that
the interventions above may inuence this relationship,
thereby requiring periodic assessment of the distal blood
pressure at full occlusion, to again re-establish the zero-ow
state. Using this principle of targeting a ow range based on
the pressure below the level of the balloon enables clinical
implementation of REPO in the absence of direct aortic ow
measurements.
REPO has been explored in multiple large animal models
with varying durations of controlled and uncontrolled hemorrhage and ischemia. In our initial proof-of-concept experiments, REPO was performed using a largely experimental
construct, whereby blood was shunted through a custom
extracorporeal ow circuit in order to tightly regulate ow.
This study utilized a highly lethal liver injury model, that
resulted in uniform demise in the absence of intervention. Following a brief period of complete aortic occlusion
(20 minutes), animals underwent either 70 minutes of continued complete aortic occlusion or REPO (150–300 mL
per minute blood ow; approximately 5%–10% of baseline
native aortic ow). This prolonged intervention period was
140 SECTION 3 • Emerging Technologies and New Approaches to Vascular Trauma and Shock
Kaplan-Meier survival estimates
Time (hours)
Animals surviving (%)
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Fig. 12.4 Relationship of proximal and distal mean arterial blood pressure to aortic flow beyond the level of flow restriction. Note that distal mean
arterial pressure (MAP) and aortic flow correlate across iterative levels of hemorrhage. This correlation does not exist between proximal mean arterial
pressure and aortic flow across various levels of hemorrhage.
chosen to simulate the reality of modern tactical evacuation
on the battleeld, recognizing that application of complete
REBOA is not feasible in scenarios where prolonged intervention (greater than 60 minutes) is required. Following
the uncontrolled hemorrhage period, animals underwent
denitive hemorrhage control and a protocolized critical
care period, where uid or vasopressor administration/
titration was determined autonomously via an algorithm
based on continuous hemodynamic monitoring. The differences were striking. All but one REPO animal survived
the intervention period, with the remainder surviving the
duration of the critical care period, compared to only 50%
survival for the group who was subjected to 90 minutes of
complete aortic occlusion (Fig. 12.5).
11
Importantly, this study demonstrated that blood ow to
the lower torso as low as 10% of baseline ow using the
REPO approach was sufcient to offset the deleterious effects
of sustained aortic occlusion, including distal ischemia and
the supraphysiologic proximal aortic pressure and cardiac
afterload induced by sustained complete aortic occlusion.
To evaluate for benet of REPO for durations of intervention closer to what could be anticipated during a typical inhospital scenario, we investigated REPO over a 45-minute
intervention period using a controlled hemorrhage model. In
this study, critical care interventions were delivered entirely
autonomously based on protocolized computer-controlled
algorithms and programmable infusion pumps.13 Additionally, through continued technological development, REPO
was performed using a computer-controlled syringe pump
and a readily available, off-the-shelf compliant aortic balloon
catheter. Even for this shorter intervention duration, we saw
signicant improvement with REPO over complete REBOA
for a host of outcome measures. During intervention, REPO
animals experienced proximal mean aortic pressures (MAP)
closer to normal physiologic range as compared to REBOA.
During the critical care phase, REPO animals maintained
an average proximal MAP within the goal range and had a
higher overall MAP throughout this time period compared to
REBOA animals. REPO also resulted in aortic ow rates closer
to baseline values, thereby minimizing the hyperemia from
low systemic vascular resistance commonly experienced
100
80
60
40
20
0
0123
Fig. 12.5 Kaplan-Meier survival estimates. Regional perfusion optimization (REPO) resulted in a 90%-survival at the end of the study period,
compared to only 50% of the complete aortic occlusion arm resuscitative endovascular balloon occlusion of the aorta (REBOA). The time of
damage control surgery is denoted by the dashed vertical line. The liver
injury was uniformly fatal in the absence of intervention, with rapid
death of all control animals.
Damage
control
surgery
REBOA
REPO
CONTROL
45
with ischemia-reperfusion injury. Similarly, REPO reduced
the resuscitation requirements for uid and vasopressors
substantially and resulted in lower peak and nal lactate
levels, providing both indirect and direct evidence of a lower
ischemic burden with this approach.
Another group has provided data in support of our ndings, showing that 500 mL per minute could be tolerated
with acceptable hemorrhage volumes over extended durations of REPO, with uniform survival following hemorrhage
control and resuscitation.
14
Beyond the effects on distal vascular beds, REPO may provide benecial effects on proximal organs as well. In a 2019
study, our group explored the effects of REPO with EVAC
compared to complete REBOA on cardiac performance
as measured via preload recruitable stroke work (PRSW;
a preload-independent measure of cardiac contractility),
12 • Endovascular Variable Aortic Control 141
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obtained using high delity pressure-volume loop measurements from the left ventricle. This study demonstrated signicantly reduced cardiac strain with REPO (Table 12.2).15
It is hypothesized that REPO reduces overall cardiac work
and strain in part by reducing cardiac afterload. Our observations also suggest that catecholamines elaborated systemically in response to profound distal hypotension may
result in a disproportionate increase in cardiac output during complete occlusion, further magnifying the adverse
impact on cardiac function.16 Although benecial effects on
proximal vascular beds have been demonstrated with REPO,
it should be emphasized that a strategy to specically target
optimization of proximal hemodynamics will compromise
the ability to tightly regulate distal blood ow. For example,
if severe proximal hypertension is still present despite allowing low-level downstream blood ow with REPO, further
balloon deation to mitigate this proximal hypertension
will inherently increase downstream blood ow and may
incite rebleeding. This may be an acceptable tradeoff based
on the scenario, such as when there is concomitant vascular or pulmonary injury above the diaphragm and when
ready access to blood products allows for the increased risk
of recurrent hemorrhage.
LIMITATIONS OF REPO WITH EVAC AND
ALTERNATE APPROACHES
The experience with EVAC and REPO to date has been in
applied research models. It remains unclear if the results
of these early studies will translate into benecial outcomes
for human victims of trauma. Nonetheless, it is clear that
REBOA has limitations and requires renement in order
to optimize outcomes, which renders approaches such as
REPO with EVAC the rational next step for technologic development. It is also unclear as to whether or not modeling
ow based on pressure will be sufcient for clinical use. It
is clear from our experience that the distal pressure/ow
relationship is imperfect and will only serve as an estimate of
aortic ow, yet it is equally unclear if the delity achieved in
the lab is required to achieve acceptable clinical outcomes.
Further work is needed in this regard.
Other groups have also proposed the use of intermittent
REBOA (iREBOA) as a viable clinical strategy to overcome
some of the technical demands imposed by REPO with
EVAC, namely the need to achieve stable low-volume ow.
This approach involves cyclically deating and re-inating
the balloon based on either a specied duration or by the
resulting hemodynamic response. Reassuring large animal
studies have suggested iREBOA may signicantly expand the
duration of intervention to at least 120 minutes; however,
the ability of humans to tolerate the massive hemodynamic
uctuations that occur with this approach is of signicant
concern.
17,18
Moreover, there is signicant risk that any stable clot may become disrupted with an immediate return to
a full ow state upon balloon deation. Whereas the binary
state of this approach (inated or deated) is technically
simple to achieve, there remains a signicant demand by
the provider to constantly assess the balloon and the resultant hemodynamics. It also creates a challenge in terms
of negotiating the management of unstable hemodynamics. It would be challenging to distinguish if hypotension
upon deation was secondary to low distal vascular tone,
whereby balloon ination and/or vasopressor administration would be appropriate or if there was re-bleeding that
warranted immediate blood transfusion. This instability
and uncertainty does not simplify the process and may create a more unpredictable situation from a clinical decisionmaking standpoint. Nonetheless, this approach may serve
to unburden the provider from the manual aspects of balloon manipulation. Automated technology such as EVAC
has been employed experimentally to achieve this type of
cyclical balloon ination and deation.
Table 12.2 Cardiac Function of Animals in the Zone 1 REBOA, Zone 1 REPO, and Control Groups
Parametric data presented as mean ± standard deviation and nonparametric data presented as median (interquartile range)
CARDIAC OUTPUT
At end hemorrhage, L/min 4.3 ± 2.4 4.8 ± 2.0 5.0 ± 1.4 0.93
At end intervention, L/min 8.2 ± 2.1 11.3 ± 5.1 6.7 ± 2.8 0.11
End of study, L/min 6.8 ± 6 11.2 ± 6.5 7.1 ± 3 0.37
EJECTION FRACTION
At end hemorrhage, % 52 ± 11 49 ± 12 58 ± 8 0.93
At end intervention, % 57 ± 5 49 ± 12 46 ± 9 0.14
End of study, % 45 ± 11 58 ± 15 52 ± 12 0.13
ESPVR
Baseline 1.03 (0.87–1.11) 0.81 (0.68–1.33) 1.13 (0.90–1.50) 0.50
Time 74 minutes 1.85 (1.31–2.11) 2.73 (1.79–3.59) 2.45 (2.42–3.41) 0.08
End of study 1.09 (0.74–2.02) 1.39 (0.93–2.29) 2.04 (1.55–4.08) 0.28
PRSW
Baseline 44.4 (42.0–62.6) 49.1 (42.1–56.4) 51.8 (40.1–63.7) 0.85
Time 74 min 67.1 (62.7–87.9) 111.2 (102.5–148.6) 116.7 (116.6–141.4) 0.04
End of study 65.8 (41.9–80.2) 66.0 (38.8–77.1) 105.3 (84.0–119.5) 0.01
ESPVR, End systolic pressure volume relationship; PRSW, preload recruitable stroke work; REBOA, resuscitative endovascular balloon occlusion of the aorta;
REPO, regional perfusion optimization.
Control Group (n = 6) Zone 1 REBOA Group (n = 6) Zone 1 REPO Group (n = 6) P Value
142 SECTION 3 • Emerging Technologies and New Approaches to Vascular Trauma and Shock
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Fig. 12.6 Endovascular variable aortic control (EVAC) hardware platform. (A) External view of the custom wireless EVAC controller. (B) Internal view.
(C) Automated EVAC syringe pump in use during a representative experiment. (Reprinted from Williams et al. A novel automated endovascular variable
aortic control device to expand function of standard REBOA catheters. JEVTM. 2019;3:3–10.)
Future Directions
Our group has rened a viable strategy to achieve controlled,
titrated distal aortic ow using conventional compliant balloon catheters inated with a prototype-grade automated
syringe pump. This pump and its associated controller, which
automate the process of balloon ination and deation using
closed-loop feedback, represent a major advancement forward (Fig. 12.6).4 The automated syringe pump is capable
of making microliter-sized balloon volume adjustments in a
near continuous fashion. However, further technique renement and technological development is required to translate
REPO with EVAC into a clinically viable therapy.
EVAC is imminently achievable using conventional pressurebased hemodynamic monitoring, yet the process would be
more streamlined if it were feasible to directly measure
ow beyond the balloon. There are a variety of established
catheter-based technologies that could be employed to enable
this. With a broader endorsement of the merits of ow-based
resuscitation strategies, this technologic development may
become justied.
Disclosure
Dr. Williams is a co-founder of and consultant for Certus
Critical Care, Inc., actively developing EVAC technology and
other critical care robotics.
References
1. Bif WL, Fox CJ, Moore EE. The role of REBOA in the control of
exsanguinating torso hemorrhage. J Trauma Acute Care Surg.
2015;78:1054–1058.
2. Russo RM, Neff LP, Johnson MA, Williams TK. Emerging endovascu-
lar therapies for non-compressible torso hemorrhage. Shock. 2016;
46(3 suppl 1):12–19.
3. Russo RM, Neff LP, Lamb CM, etal. Partial resuscitative endovascular
balloon occlusion of the aorta in swine model of hemorrhagic shock.
J Am Coll Surg. 2016;223:359–368.
4. Williams T, Nef f LP, Tibbits EM, etal. A novel automated endovascular
variable aortic control device to expand function of standard REBOA
catheters. JEVTM. 2019;3:3–10.
5. DuBose RJ. “What’s in a name?”: A consensus proposal for a common
nomenclature in the endovascular resuscitative management and
REBOA literature. JEVTM. 2017;1(1).
6. Johnson MA, Williams TK, Ferencz SE, etal. The effect of resuscitative
endovascular balloon occlusion of the aor ta, partial aortic occlusion
and aggressive blood transfusion on traumatic brain injury in a
swine multiple injuries model. J Trauma Acute Care Surg. 2017;83:
61–70.
7. Johnson MA, Neff LP, Williams TK, DuBose JJ, Group ES. Partial
resuscitative balloon occlusion of the aorta (P-REBOA): clinical
technique and rationale. J Trauma Acute Care Surg. 2016;81:S133–
S137.
8. Davidson AJ, Russo RM, Ferencz SE, etal. Incremental balloon dea-
tion following complete resuscitative endovascular balloon occlusion
of the aorta results in steep inection of ow and rapid reperfusion in
a large animal model of hemorrhagic shock. J Trauma Acute Care Surg.
2017;83:139–143.
9. Russo RM, Williams TK, Grayson JK, etal. Extending the golden hour:
partial resuscitative endovascular balloon occlusion of the aorta in
a highly lethal swine liver injury model. J Trauma Acute Care Surg.
2016;80:372–378.
10. Williams TK, Tibbits EM, Hoareau GL, et al. Endovascular vari-
able aortic control (EVAC) versus resuscitative endovascular
balloon occlusion of the aorta (REBOA) in a swine model of hemorrhage and ischemia reperfusion injury. J Trauma Acute Care Surg.
2018;85:519–526.
11. Williams TK, Neff LP, Johnson MA, etal. Automated variable aortic
control versus complete aortic occlusion in a swine model of hemorrhage. J Trauma Acute Care Surg. 2017;82:694–703.
12. Johnson MA, Davidson AJ, Russo RM, etal. Small changes, big effects:
the hemodynamics of partial and complete aortic occlusion to inform
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next generation resuscitation techniques and technologies. J Trauma
Acute Care Surg. 2017;82:1106–1111.
13. Johnson MA, Tibbits EM, Hoareau GL, etal. Endovascular perfusion
augmentation for critical care: partial aortic occlusion for treatment
of severe ischemia-reperfusion shock. Shock. 2019;51:659–666.
14. Forte D, Do WS, Weiss JB, et al. Titrate to equilibrate and not
exsanguinate! characterization and validation of a novel partial
resuscitative endovascular balloon occlusion of the aorta catheter in
normal and hemorrhagic shock conditions. J Trauma Acute Care Surg.
2019;87:1015–1025.
15. Beyer CA, Hoareau GL, Tibbits EM, etal. Resuscitative endovascular
balloon occlusion of the aorta (REBOA) induced myocardial injury
is mitigated by endovascular variable aortic control (EVAC). J Trauma
Acute Care Surg. 2019;87:590–598.
16. Hoareau GL, Williams TK, Davidson AJ, et al. Endocrine effects of
simulated complete and partial aortic occlusion in a swine model of
hemorrhagic shock. Mil Med. 2019;184:e298–e302.
17. Kuckelman JP, Barron M, Moe D, et al. Extending the golden hour
for Zone 1 resuscitative endovascular balloon occlusion of the aorta.
J Trauma Acute Care Surg. 2018;85:318–326.
18. Morrison JJ, Ross JD, Houston Rt, Watson JD, Sokol KK, Rasmussen
TE. Use of resuscitative endovascular balloon occlusion of the aorta
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2014;41:130–137.
13
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Selective Aortic Arch Perfusion
JAMES E. MANNING and ED B.G. BARNARD
Introduction
Selective aortic arch perfusion (SAAP) is an emerging
endovascular resuscitation technique that provides temporary extracorporeal perfusion to the heart and brain
during cardiac arrest.1 The aim of SAAP is to reverse the
cardiac arrest, resulting in restoration of intrinsic cardiac
output with a palpable pulse (a return of spontaneous circulation [ROSC]), with a good neurological outcome. SAAP
was developed specically as a cardiac arrest therapy and
is applicable to both medical cardiac arrest (sudden cardiac
death) and hemorrhage-induced (including traumatic)
cardiac arrest. The series of SAAP interventions (SAAP
modalities) provides a stepwise escalation of aortic balloon occlusion and extracorporeal perfusion that generates
higher blood ow than that achieved by closed-chest cardiopulmonary resuscitation (CPR). The sequence of SAAP
modalities are used to achieve a ROSC, or to provide bridging
heart and brain perfusion support until cannulation for prolonged venoarterial extracorporeal life support (VA-ECLS) if
required. The ability to escalate sequentially through these
SAAP modalities has potential utility to better inform the
complex risk:benet decision-making of resuscitation interventions in states of severe hemorrhagic shock and cardiac arrest. This chapter will include a description of SAAP
and its sequential escalating interventions, the rationale
for SAAP in clinical practice, a summary of large-animal
laboratory data, an explanation of how SAAP complements
other endovascular resuscitation techniques, and the implications for trauma and vascular surgery.
steady infusion of perfusate to maintain aortic valve closure
(Fig. 13.3). This step is important, as failure to close the aortic valve can lead to regurgitation of the perfusate into the
left ventricle, left atrium, and pulmonar y venous system limiting the benecial effects of SAAP therapy in cardiac arrest.
After the initial bolus, the infusion rate requi red to maintain closure of the aortic valve can be lower: 10 mL/kg/min
has been used in most of the laboratory research studies to
date. The key to maintaining competent aortic valve closure
is that the subsequent infusion must begin immediately
after the bolus, thereby not allowing the aortic pressure to
drop and the aortic valve to open.
The initial perfusate is preferably an exogenous oxygen
carrier, such as stored (allogeneic) whole blood or packed
red blood cells, or a non-blood product, such as a hemoglobin-based oxygen carrier (HBOC) or a peruorocarbon
(PFC) emulsion. The perfusate is passed through an oxygenator and infused using a pump system. Centrifugal pumps,
roller-wheel pumps, and peristaltic pumps have all been
used successfully to perform SAAP in laboratory models.
Limited experiments to date have also shown that rapid
serial boluses performed manually are also effective, but
the overall perfusion rate is lower than mechanical pump
continuous infusion and the time required to achieve ROSC
is generally longer. Nonetheless, in austere environments—
such as military theaters and some prehospital settings—
manual infusion for SAAP may prove to be most practical.
The Rationale for SAAP
A Description of SAAP
SAAP uses a large-lumen, balloon occlusion catheter
inserted into a femoral artery and advanced to the level
of the descending thoracic aorta with an insertion length
based on body surface measurement (femoral insertion siteto-umbilicus-to-xyphisternal junction). This method positions the SAAP catheter balloon in the aorta between the
diaphragm and the left subclavian artery (Fig. 13.1). This
leeway in balloon position within the descending thoracic
aorta allows for insertion and initiation of resuscitative perfusion without the need for imaging technology to verify
balloon location (Fig. 13.2A,B). When the SAAP catheter
balloon is inated, the aortic arch vessels, including the coronary, carotid, and vertebral arteries, are relatively isolated
for perfusion with an oxygenated perfusate via the central
infusion lumen of the SAAP catheter.
After the SAAP catheter balloon is inated, an initial rapid
bolus of perfusate (50 mL/2–3 seconds) into the aortic arch
is used to close the aortic valve, followed immediately by a
144
CARDIAC ARREST SURVIVAL
Cardiac arrest is a major public health problem in the
United States and throughout the world. According to a
2015 Institute of Medicine Report, there are an estimated
600,000 cardiac arrests each year in the United States
alone.2 This includes cardiac arrest due to primary cardiac
causes as well as trauma, poisonings, and other etiologies.
Of these, approximately 395,000 occur outside of a hospital setting and the survival rate overall for this population
is less than 8%.
pital cardiac arrests each year with a survival rate of about
2,4
24%.
medical cardiac arrest are the inadequate myocardial blood
ow produced by closed-chest CPR, delays in initiation of
bystander CPR, and lack of early debrillation.
1
mated to be 60,000 cases/year in the United States.5 Reported
survival in traumatic cardiac arrest (TCA) is improving but
may be even lower than medical cardiac arrest—many of the
potentially survivable deaths are due to exsanguination.
The major limiting factors in achieving a ROSC in
The incidence of cardiac arrest secondary to trauma is esti-
2,3
There are an estimated 200,000 in-hos-
5,6
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