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66
Zero point survey
Identify team goals and set mission trajectory
C. Hicks and A. Petrosoniak
positive social interactions within teams is establishing a sufcient sense of psychological safety: that is, that the team
environment is safe for interpersonal risk-taking [6].
Psychological safety is correlated with improved safety
behaviors like error reporting and promotes knowledge and
power sharing, cogeneration and team learning [7].
Fostering psychological safety requires all team members, and perhaps most notably the team leader, to admit
uncertainty, express doubt, seek input, and ask for help.
Traditional models of team leadership that call upon the
team leader to assume an all-seeing, all-knowing posture are
counterproductive to establishing psychological safety and
quite often call upon the team leader to compensate for these
vulnerabilities by assuming an authoritative and at times
authoritarian posture. Such negative emotional valence rapidly translates to the remainder of the team, a concept
described by Soares and Lopes as emotional contagion [8].
Conversely, by openly embracing vulnerability and uncertainty when it exists, emotional contagion can be harnessed
to generate more positive attitudes and behaviors, including
voicing concern, cooperation, collaboration and mutual support. Creating a robust sense of psychological safety is the
means by which the positive attributes of an inter- professional
team may be brought to bear, cueing and facilitating the
transactive memory of a diverse group of team members
towards a common and shared goal [1]. Far from displaying
weakness, team leaders who are willing to admit uncertainty
and appreciate their limitations are generally regarded as better and more effective than those who do not.
Team leaders can foster psychological safety in several
concrete ways. Seeking team input by asking “What am I
missing?” sends a powerful message that the leader is willing
to both admit uncertainty and seek input. Clearing cognitive
dissonance by articulating ambiguity may also help realign
mental models by provoking a conversation about next best
steps: “The patient didn’t respond as expected to a volume
challenge, raising the possibility that other causes of shock
might be in play; I seek your input on what our immediate next
steps should be.” Opportunities to build psychological safety
are multiple and include the pre-primary survey (the ZeroPoint Survey), during pre-briengs, and at set check-in or
recap points that occur as the resuscitation progresses.
The Zero-Point Survey
In an organized resuscitation, the primary survey should be
preceded by a series of steps to ensure self, team, and environmental preparation. Ideally, effective teams start preparing to resuscitate before patients arrive.
The Zero-Point Survey (ZPS) is a consensus-derived
framework for organizing pre-primary survey discussions
around self, team, and environmental preparation [9]. The
ZPS is designed to create shared mental models and facilitate
implicit coordination by direct team-based discussion and
preparation prior to patient arrival, and is updated periodically once the resuscitation commences. The STEP-UP mnemonic is used to recall the elements of the ZPS (Fig.11.1).
Although diagrammed as a linear process, the interplay
between elements of the ZPS (e.g., self and team) necessitates
a back-and-forth reappraisal as the scenario progresses.
Prior to patient arrival, team members are prompted to
examine and appraise their own sense of psychological
preparedness, or fitness to execute via I’M SAFE (Illness,
Medication, Stress, Alcohol, Fatigue, Eating/
Elimination), with the implication that reversible incumbrancers to individual performance are identified and
addressed, or partially mitigated before engaging in
patient care. This is followed by a focused examination
of roles, anticipated early priorities, and an environmental scan for equipment safety and logistics. Environmental
preparation should occur well in advance, but in the
immediacy of a pending resuscitation team members
should at a minimum be made aware of the location of
and anticipate the need for key equipment and planned
pathways for patient and team member movement. Nonclinical personnel should be assigned specific roles to
support clinical logistics, including equipment gathering,
layout, and patient positioning.
A pre-primary survey facilitates the creation of robust
shared mental models; a mental model is shared when that
same cognitive representation is mutually understood and
acknowledged between team members [5]. As a dynamic
event progresses, the mental model needs to be periodically
updated to incorporate new data and changing priorities. A
structured Zero-Point Survey can help to clarify elements of
Pre-resuscitation
S
Self
Physical readiness: I’M SAFE
Cognitive readiness: breathe, talk, see, focus
T
Team
Leader identified
Roles allocated
Briefing
Repeat as non-
clinical situation
changes
Fig. 11.1 Zero-Point Survey and the STEP-UP mnemonic
E
Environment
Danger, space, light, noise, crowd control
Resuscitation commenced
P
Patient
Primary survey ABCDE
U Update
Share mental model of patient status
P
Priorities
Repeat as clinical
situation changes
11 The Trouble withTeams: Practical Tools forComplex Trauma Team Dynamics
an ambiguous clinical event, allow for team input and
challenge- response queries, and allow the team leaders to
establish early goals and priorities.
The resuscitation environment can be hazardous for providers, and in many situations, team hazards are accepted as
an unavoidable or unnoticed element of resuscitation practice. In many cases, a simple and focused environmental and
equipment scan can help identify and mitigate latent safety
hazards before they can inict harm. This may include the
provision of adequate lighting, positioning and spacing of
procedure trays and carts in relation to the provider, positioning the stretcher centrally to ensure 360-degree patient access,
and unencumbering monitoring wires and sterile equipment.
Once the patient arrives and the primary survey commences, adjustments to team structure, composition, and
environment will invariably be required in response to
Fig. 11.2 The four-point trauma pre-brief: conducted in under a minute, led by the nurse co-lead, focusing on early and immediate
priorities
dynamic patient needs. Assigning a logistics and safety
officer—someone other than the clinical team leader—
can assist with managing clinical logistics and optimizing the safe and efficient execution of clinical tasks. This
is separate from clinical oversight and task prioritization
and may include crowd and noise control, patient positioning, equipment logistics, safe movement of clinical
personnel, and planning for patient egress. The importance of the safety officer has been highlighted in recent
years by the need to monitor personal protective equipment protocols in light of emergent infectious diseases
like COVID-19 [10].
discuss early anticipated priorities (blood, airway management, chest trauma), what is needed to address those priorities (massive hemorrhage protocol, difcult airway setup,
nger thoracostomy cart), and roles (who will do what).
Importantly, our pre-briengs are nurse-led, a modication
that helps to establish our preferred nurse-physician co-lead
trauma team model.
Transitions in care (patient hand-offs or sign-over) are
high-risk periods in patient care. Standardized sign-over
protocols can improve data transfer and ensure a smooth
transition between care teams. This is of particular relevance to sign-over between pre-hospital and trauma teams,
Briengs andChecklists
wherein the need for repetition is associated with degradation in both the quality and quantity of information trans-
Structured briengs can help create psychological safety
by clarifying what is known, and by extension what
remains unknown about a clinical scenario and provide an
avenue for team members to ask questions and request
clarication ahead of engaging in the hands-on work of the
primary survey. Team-based pre-brieng—which takes
place prior to patient arrival—is an effective way to establish relational coordination within an ad hoc team.
Relational coordination theory refers to elements of teamwork that facilitate optimal functioning and are characteristic of high-performance organizations and teams and
includes shared knowledge and goals that go beyond an
individual’s task-specic requirements, understanding
how a team member’s role integrates into the broader team
framework, and establishing mutual respect as a means of
facilitating psychological safety [11].
An ideal pre-brieng is rapid, team-based, and focused
on immediate roles and priorities. At our trauma center, we
use a four-question pre-brief in challenge-and-response format (Fig.11.2). The intent is to quickly establish what is
known (mechanism, injuries, clinical status, arrival time),
ferred [12]. We emphasize a hands-off, eyes-on approach to
sign-over, whereby team members refrain from engaging
with the patient while sign-over takes place. The exception
is when sign over and active resuscitation must take place
concurrently; A balance between the two may include asking the prehospital team “Do you have any concerns that
require our immediate attention before we proceed with
sign-over?”
Checklists can help integrate safety behaviors into both
standard and non-standard operations in situations where
omissions are otherwise common, high stakes, or both.
When used correctly, checklists can force-function elements of care that might otherwise be bypassed. The
World Health Organization (WHO) has developed a
trauma care checklist that we have modied according to
identied local needs [13]. In our trauma center, we use
the modied WHO checklist as a pre-departure review
prior to egressing from the trauma bay to summarize key
tasks, seek input from team members, and ensure adequate preparations have been made to facilitate patient
movement (Fig.11.3).
67
68
10
11
12
14
15. Are there ANY CONCERNS or ISSUES from any team member?
C. Hicks and A. Petrosoniak
tication stickers placed over top of personal protective
Pre-Departure Checklist
1. Is there potential for further airway compromise?
If yes, has the airway been SECURED prior to departure?
2. Have we reviewed Chest and Pelvis X-RAYS?
3. Is the patient in SHOCK? If YES, have we notified the TRAUMA SURGEON?
equipment may in part help to address this.
(ii) Resuscitation lexicon. Yamada etal. have proposed the
development of a lexicon of short words or phrases that
succinctly communicate commands and requests, similar to what is used by cockpit crews [14]. Examples
include conrm (“Conrm pre-hospital systolic blood
pressure was 70 mmHg”), I say again (“I say again:
carotid pulse is absent”), request (“Request update on
4. Are BLOOD products required or the MHP needed?
Indicators: > 4U blood products in 1hr OR ABC Score > 2 OR evidence of shock
5. Have we controlled EXTERNAL bleeding?
6. Is Tranexamic Acid indicated?
If YES, administer 2 grams IV
7. Have we recorded TEMPERATURE and treated hypothermia (T < 35°C)?
volume status”), and read-back (“Please read back the
total count of blood products given”).
(iii) Closed-loop communication. Closed-loop communication
has three steps—directing an order or request to a specic
individual, and having that request verbally acknowledged
as both received and completed successfully [15]. The
third step is the most challenging, as complete is not synonymous with completed correctly. Effective closed-loop
8. Have we considered ANALGESIA, antibiotics and tetanus?
9. Have we documented the NEUROVASCULAR status of all 4 limbs?
. Is VASCULAR ACCESS adequated and functional?
communication, therefore, requires cross-monitoring and
mutual support amongst team members, with a particular
emphasis recognizing when an action or intervention does
not achieve the predicted result.
(iv) Graded assertiveness. The two-challenge rule is meant
. Do we have all MEDICATIONS necessary for TRANSPORT?
. Do we have the TRANSPORT MONITOR connected and functioning?
to counteract authority gradients and provide a structured means for expressing concern about a plan of
action in a graded fashion [16]. The two-challenge
13. Have we updated the FAMILY?
. Have we contacted the RECEIVING UNIT?
C-U-S framework begins with directly stating a concern (“I am concerned about using paralytics for this
difcult airway”). If the desired result is not obtained,
the next step is for a team member to identify they are
Fig. 11.3 Our trauma pre-departure checklist
uncomfortable moving forward with the plan as outlined (“I am uncomfortable paralyzing this patient given
the presence of severe airway trauma”). Finally, a safety
Language andTeam Coordination
issue is declared if the plan moves forward without ade-
quate modication or retraction (“We must pause here
Verbal and non-verbal communication set the tone for how a
team performs and responds, particularly when time pres-
as this is unsafe; I will ask another senior physician to
assist us in nding a path forward”).
sures mount and opportunities for error and ambiguity are
abundant. Issues with communication arise in virtually every
critical event debrieng, and yet there is surprisingly little
attention paid to known and effective techniques for effective
Tactical Pauses, Sit-Reps andSnap Briefs
crisis communication.
As the resuscitation progresses, the mental model needs to
(i) Mitigating language. Mitigating phrases are the often-
subconscious choice of language that downplays or
minimizes the meaning of what is being said. This
includes phrases like “Could we place a chest tube?” or
“Could someone draw up medications for RSI?” which
are better rephrased as the commands they are intended
to be: “Please perform a right-sided nger thoracostomy,” “Mark, draw up 100mg of ketamine.” Concise
and direct should not be thought of as synonymous with
impolite or offensive. Not knowing names and roles can
at times present a barrier to direct and non-mitigating
communication; the introduction of name and role iden-
be updated in an equally concise fashion. Led by the team
leader, a tactical pause is a break in case action in order to
summarize, reect, and set priorities for next stages in care.
During a tactical pause, all non-essential clinical activity
stops and all team members listen, reect, and are asked to
respond as needed. 10in 10 snap briefs involve 10-second
updates provided by the team leader every 10minutes and
include a brief recap of the case, clinical events happening
now, anticipated next steps and priorities, and role allocation
or clarication (Table11.1) [2].
Tactical pauses should go beyond one-way data transfer
from leader to team but actively seek input from team mem-
11 The Trouble withTeams: Practical Tools forComplex Trauma Team Dynamics
69
Table 11.1 The 10-in-10 snap brief model
1. Recap on what has been achieved (or not) do far
2. What’s happening now
3. Agree next most important steps
4. Prioritize next steps (with indicative timelines if possible e.g. we
need to be ready to go scan in 10minutes)
5. Allocate specic people/kit/resource to achieve next steps
bers. This pause in the action provides an opportunity for
team members to speak up about questions, observations, or
concerns, provided there is sufcient psychological safety
for them to feel comfortable doing so.
Adaptive Coordination
Teams that participate in team training augmented with regular pause and reassess situation updates are better able to
maintain exible mental models, utilize more effective
forms of communication, and are more resilient to the inuence of acute stress on performance. Adaptive coordination
refers to a team’s ability to predict and modify their behavior in response to dynamic clinical and environmental
cues—in other words, this is how mental models and transactive memory are operationalized [17]. Entin and Serfaty
examined the performance and communication strategies of
ve-member naval ofcer teams during anti-air warfare
exercises under a number of experimental training conditions [3]. Teams whose leader periodically provided situation-assessment updates—sit reps—to summarize priorities
and current situation assessment demonstrated better teamwork and task completion and were more resilient to the
effects of stress and task load. In fact, teams that were armed
with the combination of team training and a pause and reassess framework that included periodic sit-reps were the only
experimental group to maintain their performance in the
face of increasing task burden, with task overload used as a
proxy for acute stress. This phenomenon will be familiar to
anyone who has participated in a trauma resuscitation
involving multiple injuries or multiple casualties: as time
pressure mounts and task demand is high, high-performing
teams need to be armed with specic strategies to maintain
performance as demands begin to outstrip resources.
Tipping the stress appraisal from threat to challenge is a key
facet of what adaptive coordination training seems to
accomplish.
In Entin and Serfaty’s study, teams using sit-reps shifted
from explicit to implicit modes of communication—that is,
team members shared information with team members more
frequently and directly, without having been asked to do so.
This observation is consistent with the ability to anticipate the
needs of fellow team members—a key feature of expert team
performance. Translated to clinical practice, adaptive team
behaviors are facilitated by team leaders who periodically pause
and reassess to openly share information, summarize data, voice
specic ndings, and seek team input and feedback.
Making It Happen
The drive toward implicit coordination and expert team performance requires focused practice in addition to understanding the theory. Interprofessional team training by way
of in situ simulation—simulation training that takes place in
the physical workspace itself—is a powerful tool to drive
home key knowledge, skills, and attitudes relevant to team
performance. Opportunities for in situ simulation abound,
from building living morbidity and mortality rounds based
on difcult prior cases, to just in time simulation focusing on
a discreet and manageable element of team behaviors. In our
trauma center, simulation has played a key role in shaping
elements of trauma team culture, from designing the environment to integrating pre-briengs into standard operating
procedures. And beyond simulation, debrieng after live
clinical events allows for the identication and mitigation of
safety hazards—team-based, environmental, and systemic—
that would otherwise go unnoticed or uncorrected.
To be successful, teams must be situated in an organizational framework that supports the importance of team training. Teams don’t exist in a bubble, and the complex
interprofessional work of a trauma team is much more likely
to succeed when organizations show overt and explicit support for team training [18]. In a system predicated on individual resilience, the onus is on organizational leadership to
ensure top-down support to push the envelope of trauma
team performance.
Key Notes
• Effective teamwork is not intuitive, as a team of
experts does not make an expert team; instead, they
rely on specic training and actions to create a
high-performance trauma team.
• Elite trauma team performance employs a combination of actions and concepts, including implicit
coordination, psychological safety, briengs and
checklists, adaptive coordination, and effective
language.
• Interprofessional team training by way of in situ
simulation—simulation training that takes place in
the physical workspace itself—is a powerful tool to
drive home key knowledge, skills, and attitudes relevant to team performance.
• In a system predicated on individual resilience, the
onus is on organizational leadership to ensure topdown support to push the envelope of trauma team
performance.
70
C. Hicks and A. Petrosoniak
References
1. Nawata K, Yamaguchi H, Aoshima M. Team implicit coordination based on transactive memory systems. Team Perform Manag.
2020;26(7/8):37–390.
2. Carley S.Five free strategies to improve your Resus Room 2018.
St Emlyn’s Blog. https://www.stemlynsblog.org/stemlynslive- ve-
free- strategies- to- improve- your- resuscitation- practice- st- emlyns/.
Accessed 10 Sept 2022.
3. Entin EE, Serfaty D. Adaptive team coordination. Hum Factors.
1999;41(2):312–25.
4. Cannon-Bowers JA, Salas E, Converse S.Shared mental models in
expert team decision making. In: Castellan Jr NJ, editor. Individual
and group decision making: current issues. Hillsdale: Lawrence
Erlbaum Associates, Inc; 1993. p.221–46.
5. Mathieu J, Heffner TS, Goodwin GF, etal. The inuence of shared
mental models on team process and performance. J Appl Psychol.
2000;85(2):273–83.
6. Delizonna L. High-performing teams need psychological safety:
here’s how to create it. Harv Bus Rev. 2017. https://hbr.org/2017/08/
high- performing- teams- need- psychological- safety- heres- how- tocreate- it. Accessed 10 Sept 2022.
7. Kim S, Lee H, Connerton TP.How psychological safety affects
team performance: mediating role of efcacy and learning behaviour. Front Psychol. 2020;11:1581.
8. Soares AE, Lopes MP.Social networks and psychological safety: a
model of contagion. J Ind Eng Manag. 2014;7(5):950–1012.
9. Reid C, Brindley P, Hicks C, etal. Zero point survey: a multidisciplinary idea to STEP UP resuscitation effectiveness. Clin Exp
Emerg Med. 2018;5(3):139–43.
10. Hicks C, Bridley P.COVID-19 miniRAGE with Hicks and Brindley.
LITFL. 2020. https://lit.com/covid- 19- minirage- with- hicks- and-
brindley/. Accessed 10 Sept 2022.
11. Purdy E, Alexander C, Shaw R, Brazil V.The team brieng: setting
up relational coordination for your resuscitation. Clin Exp Emerg
Med. 2022;7(1):1–4.
12. Sanjuan-Quiles A, Hernandez-Ramon MP, Julia-Sanchis R, et al.
Handover of patients from prehospital emergency services to emergency departments. J Nurs Care Qual. 2019;34(2):169–74.
13. WHO Trauma Care Checklist. https://www.who.int/publications/i/
item/trauma- care- checklist. Accessed 10 Sept 2022.
14. Yamada NK, Fuerch JH, Halamek LP.Impact of standardized communication techniques on errors during simulated neonatal resuscitation. Am J Perinatol. 2016;33:385–92.
15. Hargestam M, Lindkvist M, Brulin C, et al. Communication in
interdisciplinary teams: exploring closed-loop communication during in situ trauma team training. BMJ Open. 2013;3:e003525.
16. Pocket Guide: TeamSTEPPS 2.0. 2013. https://www.ahrq.gov/
teamstepps/instructor/essentials/pocketguide.html#:~:text=on%20
next%20steps.- ,Two%2DChallenge%20Rule,that%20it%20
has%20been%20heard. Accessed 10 Sept 2022.
17. Burke S, Salas E, Pierce L.Understanding team adaptation: a conceptual analysis and model. J Appl Psychol. 2002;91(6):1189–207.
18. Driscoll PA, Vincent CA. Organizing an efcient trauma team.
Injury. 1992;23(2):107–10.
Biological andPsychological
Interactions oftheStress Response:
How toBuild Resilient Trauma Teams
RebeccaJ.Ryznar, ChristianClodfelder,
andJereyEdwards
12
Biological Basis fortheHuman Stress
Response
The human response to stress is a homeostatic mechanism in
place to allow humans the ability to adapt to either real or
perceived environmental stressors. The overall response to
stressors is a complex balance of many organ systems. The
modality, source, and duration of stressors produce a myriad
of dynamic physiologic responses that can be both adaptive
and maladaptive.
The discussion of the entire human physiologic response
to stress is complex and beyond the scope of what is relevant
to this text. However, a cursory understanding helps trauma
teams appreciate and manage the response that they will
inevitably face. The basic mechanisms of the human stress
response will be discussed in an acute versus chronic context
and by individual organ system.
SNS andHPA: Eectors oftheStress Response
The acute response to a stressor is an immediate, coordinated
effort by the body to adapt to a changing environment. The
primary mechanisms of initiating this response are the sympathetic nervous system (SNS)—colloquially known as the
“ght-or-ight” response—and recruitment of the
hypothalamic- pituitary-adrenal axis (HPA). Activation of
both physiologic systems occur within seconds of real or
perceived stress. The SNS and HPA axis provide elevated
energy resources and upregulate metabolic processes to
R. J. Ryznar (*)
Rocky Vista University, Englewood, CO, USA
e-mail: rryznar@rvu.edu
C. Clodfelder
University of Nebraska Medical Center, Omaha, NE, USA
e-mail: Christian.clodfelder@rvu.edu
J. Edwards
Swedish Family Medicine, Englewood, CO, USA
e-mail: Jeffrey.edwards@rvu.edu
respond to changes in the environment. They also initiate
long-term processes that eventually result in downregulation
of potentially negative inammatory responses.
The SNS is the nervous system’s mechanism for responding to stressful stimuli. It is a collection of nerves that innervate tissues in the body and release primarily the
catecholamines, norepinephrine and epinephrine, in order to
cause changes in those tissues, which promote survival in
dangerous situations. For example, the SNS activates the
heart to pump harder and faster, it constricts blood vessels to
organs so blood can be diverted away from digestive processes and toward the muscles for physical movement, and it
dilates the pupils for enhanced awareness of surroundings.
The SNS also activates the adrenal medulla, which can be
viewed as a modied SNS nerve, except instead of innervating individual tissues it releases catecholamines into the
blood stream, causing systemic sensitization to SNS tissue
signals. All of these are highly useful when the organism is
motivated to avoid danger, but it is also involved in responding to physiological stimuli that we encounter each day without realizing it, such as combatting a drop in blood pressure
when we stand up from sitting [1].
The HPA plays an important role in the stress response as
well, but while the SNS sends nerve signals to the adrenal
cortex to release catecholamines, the HPA axis sends hormonal signals to activate the adrenal cortex to release cortisol. The key players of the HPA are the paraventricular
nucleus (PVN) within the hypothalamus, the anterior pituitary gland, and the adrenal cortex. In response to stressors
via the same mechanism as the SNS, the PVN synthesizes
and releases corticotropin-releasing factor (CRF). CRF
reaches the anterior pituitary gland via the hypophyseal portal system, causing the release of adrenocorticotropic hormone (ACTH) from corticotroph cells into systemic
circulation [2]. When ACTH reaches the adrenal cortex, it
stimulates the production and release of glucocorticoids into
the blood. The glucocorticoid with the most relevance to
human physiology is cortisol. Cortisol is a steroid hormone
that interacts with glucocorticoid receptors in many tissues
© Springer Nature Switzerland AG 2025
L. Marshall Gillman, S. Widder (eds.), Trauma Team Dynamics, https://doi.org/10.1007/978-3-031-86312-7_12
71
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R. J. Ryznar et al.
of the human body. Cortisol stimulates gluconeogenesis,
glycogenolysis, and lipolysis, which together increase the
amount of glucose and fatty acids in the bloodstream for
cells and tissues to utilize. Cortisol also upregulates catecholamine receptors in arterioles, increasing their sensitivity
to epinephrine and norepinephrine and effectively raising
arterial blood pressure. Cortisol also has potent immunosuppressive and anti-inammatory effects [3, 4].
The rst step in the stress response is sensing the stressful
change in the environment. Physiologically, this is achieved
by various sensors and receptors throughout the body. Those
sensors transmit a signal to the central nervous system
(CNS), at which point they are interpreted and reacted to. It
is important to keep in mind that although there are many
types of sensory input, the stress response system still reacts
via the SNS and HPA axis, meaning different stressors have
similar effects on the body.
A sudden loss of blood pressure is an example of a “physiological stress” for which the body has developed systems
to control and maintain homeostasis. A sudden drop in blood
pressure is detected by baroreceptors in the aortic arch and
carotid sinus, and that information is communicated via general visceral afferent bers to various nuclei within the brainstem. Through a series of neural reex arcs, the SNS is
activated and information is communicated via sympathetic
nerve bers to various effector organs through the release of
neurotransmitters, classically epinephrine and norepinephrine. The end result is an increase in arterial blood pressure,
heart rate, metabolic rate, and blood glucose concentration,
thus alleviating the stress of low blood pressure. One of the
effector organs is the adrenal medulla, which can be viewed
as a modied SNS nerve that causes a massive systemic
release of epinephrine and norepinephrine, rather than just
releasing those catecholamines in a synaptic cleft. This dramatic increase in catecholamines allows for the entire body
to respond to changes quickly and simultaneously [1]. All
stressors follow this general pattern of detection, integration,
and a corrective response to a real or perceived change is
constant.
Pain is an example of a physiological stressor that we are
able to perceive; it starts with the detection of painful stimuli, such as high temperature or chemical signs of cell damage, which results in the transmission of signals through
afferent neurons. Some of these signals synapse in spinal
reex arcs, resulting in immediate withdrawal from a painful
stimulus, such as a hot ame. Others continue up into the
brain, where they are perceived as pain.
Psychological pain is a bit more complex, but it is important to note that psychological pain, often referred to as
stress, can have very similar consequences as physiological
stressors. The same effector mechanisms that regulate the
body’s response to physiological stressors control the
response to psychological and emotional stressors, leading to
increased blood pressure, decreased perfusion of vital organs,
and shifting into a catabolic state.
The amygdala, a portion of the limbic system which functions in responding to emotion, fear, and anxiety, receives
inputs from many of the sensory organs of the body. Stimuli
that the body perceives as dangerous or harmful, such as
visual and auditory perceptions, can activate the amygdala,
which in turn activates the hypothalamus and other SNS
nuclei within the brain. This results in the same downstream
effects as described above. Although acute perception of
stress is useful at times, such as the classic ancestral example
of seeing a bear and needing to run, chronic activation of this
psychological stress pathway can be quite toxic and lead to
profound mental and physical health detriments.
The limbic system, more generally, is a subset of brain
structures that are important in memory, behavior, and emotion. It is important to note that the limbic system is not considered to be the sole driver responsible for all of human
emotion and behavior. Rather, it is one of many systems that
contribute to the complex biologic concept of human emotion. Since the stress experienced by trauma teams is often
mental, emotional, or psychological—a brief discussion
about the basics of the limbic system is warranted. Within
the cerebral cortex, the limbic structures include the limbic
lobe, orbitofrontal cortex, entorhinal cortex, and piriform
cortex. The hippocampus and fornix are also cortical structures that are considered a part of the limbic system. Other
structures of the limbic system include the amygdala, septal
nuclei, nucleus accumbens, the hypothalamus, anterior
nuclei of the thalamus, and the mammillary bodies.
The hippocampus is involved in learning and memory,
and the piriform cortex is necessary for processing olfactory
information. As mentioned previously, the amygdala is one
of the better understood structures within the limbic system,
and its primary function is emotional response and decisionmaking [5]. Klüver–Bucy syndrome is a condition when a
patient has bilateral destruction of the temporal lobe—which
leads to destruction or damage of the amygdala. Initially
investigated on experiments in monkeys, monkeys that suffer
damage to the amygdala experience a complex constellation
of symptoms. The monkeys lose their fear response and react
to stimuli with lower than usual aggression. This results in a
very tame, docile affect. The monkeys also experience hyperphagia, pica, and hyperorality. Hypersexuality and visual
agnosia are also commonly described in Klüver–Bucy syndrome. The same condition has been described in human
beings, with docility, dietary changes, and hyperorality being
the most common ndings [6].
Fear and aggression have long been thought of as the primary role of the amygdala. It also is known to play a more
nuanced role in human emotional processing. There is a correlation between higher rates of mental disorders, such as
anxiety and depression, with patients who have a decit in
12 Biological andPsychological Interactions oftheStress Response: How toBuild Resilient Trauma Teams
73
certain cell types of the amygdala. These patients with
decreased concentrations of amygdala granule cells also
have lower emotional functioning compared to standard
controls.
Now that we have covered the inciting events of the stress
response, let’s discuss the downstream effects of those signals. Understanding both the short- and long-term physiologic changes is particularly valuable to emergency personnel
because recognizing and anticipating changes that occur during difcult, stressful, and traumatic situations can improve
performance and recovery.
Acute Versus Chronic Stress
The acute response to stress is regulated by negative feedback loops from downstream products like cortisol, epinephrine, and norepinephrine, which act on the adrenal gland,
hypothalamus, and anterior pituitary to suppress continued
stimulation. Normally, this negative feedback keeps the
stress response from over-activating and maintains homeostasis. Chronic stress, however, occurs when a stressful stimulus is maintained for long periods of time, such as in
repeated exposures or failures in the negative feedback loop.
Repeated exposure to stressors is viewed as a cumulative
process. Repeated or prolonged exposures to stressors cause
an HPA response and thus a cumulative increase in glucocorticoid burden, colloquially known as “too much cortisol.”
Data shows that the adrenal gland becomes both larger and
more sensitive to ACTH with repeated exposure to ACTH.For
example, there is literature demonstrating that surgical stress
can result in long-term, continuous secretion of cortisol
despite an absence of a corresponding increase in ACTH levels [7]. Additionally, immune effectors experience higher
rates of apoptosis and involution after repeated exposure to
ACTH, resulting in decreased immunological competence
and increased susceptibility to infection and cancer. It is
believed that the mechanism responsible for this increased
sensitivity to ACTH is due to downregulation of glucocorticoid receptors in the hypothalamus and other brain regions
that are necessary for negative feedback regulation [3].
It is well established that dysregulation of the HPA
(hypothalamus- pituitary-adrenal) axis is part of the underlying pathophysiology of mental health disorders, indicating
low resilience. Low resilience disorders include depression,
anxiety, PTSD, and burn out [3]. The main determinants of
HPA axis and SNS activity include genetics, early life experiences, and current life stress and other experiences [1].
Repeated stress inuences immunity by stimulating cortisol
and adrenaline secretion from the adrenal cortex and medulla,
respectively. Stress also causes the release of noradrenaline
from postganglionic sympathetic nerve terminals in blood
vessels and lymphoid organs. Glucocorticoids in turn result
in changes in the production of regulatory type 1 and type 2
cytokines (Th1 and Th2). Downstream of this process, glucocorticoids regulate physiological events and inhibit further
HPA axis activation through intracellular receptors located in
the brain and peripheral tissues [2]. More specically, this
results in suppression of pro-inammatory cytokine secretion while promoting anti-inammatory cytokine secretion
[2]. Chronic stress is associated with up-regulation of proinammatory cytokines and down-regulation of the antiinammatory cytokine pathways [3].
Stress andtheCardiovascular System
One of the most obvious and immediate effects of the human
stress response is its inuence on the cardiovascular system.
SNS effects on the heart can be either chronotropic, inotropic, or dromotropic, all of which combine to increase cardiac
output. Chronotropic refers to an increase in heart rate.
Inotropic is an increase in contractility of the myocardium.
Dromotropic is an increase in conduction velocity within the
electrical conduction system of the heart. SNS activation and
the action of catecholamines also have important effects on
blood vessels. Alpha-1 receptors cause vasoconstriction,
whereas Beta-2 receptor activation results in vasodilation.
Due to a differential distribution of these receptors on different vascular beds, blood is shunted away from the viscera
and toward the heart, lungs, brain, and skeletal muscles—
with a net overall increase in systemic vascular resistance
and blood pressure. Additionally, cortisol upregulates
Alpha-1 receptors within vascular smooth muscle cells,
increasing their sensitivity to circulating catecholamines.
The ANS and HPA axis also inuence an important cardiac parameter referred to as heart rate variability (HRV).
Specically, HRV refers to the variation in the interval
between heartbeats, specically the RR interval. In general,
decreased parasympathetic input or increased sympathetic
input will reduce the HRV, while increased parasympathetic
or decreased sympathetic input will increase the HRV [8].
In the literature describing HRV, HRV is divided into
either low frequency (0.04–0.15 Hz) or high frequency
(0.15–0.40Hz)—with low frequency referring to low HRV
and therefore more sympathetic activity, and high frequency
referring to high HRV and therefore more parasympathetic
activity. High-frequency HRV has been demonstrated to be
very clearly correlated with PSNS activity, while the connection between lower HRV and SNS activity appears to be
more complex. Knowing that different frequencies of HRV
are associated with different levels of autonomic activity, it is
often used as a rough measure for “stress” levels during exercise, simulation, or research. It is also often used as a parameter gauging the health or responsiveness of an individual’s
autonomic and cardiac function. Literature demonstrates that
74
R. J. Ryznar et al.
low HRV has been shown to be a predictor of poor outcomes
and mortality after acute myocardial infarction [9]. Patients
who are victims of sudden cardiac death have also been
found to have lower frequency HRV compared to healthy
controls. Additionally, patients who survive sudden cardiac
death are shown to have depressed HRV levels [10].
Correlations between HRV and differing outcomes in other
conditions such as heart failure, post-cardiac transplantation
outcomes, diabetic kidney disease, and susceptibility to
SIDS are also currently being explored.
It is understood that the vagus nerve is a central player in
both the parasympathetic SNS and the HPA axis. The connection between the vagus nerve and both of these systems is
bidirectional, providing both inputs and outputs that these
systems use to regulate the human stress response. As mentioned earlier, the correlation between high-frequency HRV
and PSNS activity is well described. Additionally, cortisol
levels, high-frequency HRV, and direct vagus nerve tone
have all been shown to be strongly linked. Isolated increases
in cortisol have been shown to increase resting HRV [11].
The connection and interplay between all of these physiological variables and their effect on HRV makes it an excellent
candidate for a general marker for stress levels. This could be
used to monitor stress levels on trauma teams during real life
scenarios, as well as a marker for the effectiveness of simulation and training.
The kidneys also play an intimate role in the body’s
hemodynamic and cardiovascular response to acute stressors. Activation of Beta-1 receptors in the kidneys lead to the
release of renin, eventually leading to release of angiotensin
II. Angiotensin II further increases sympathetic activity,
causes the kidneys to retain electrolytes and uid, increases
aldosterone and ADH secretion, and directly causes vasoconstriction. All of these serve to further increase blood pressure [4].
Overall, the cardiovascular response to stressors is substantial. The acute response to stress within the cardiovascular system can manifest as tachycardia, palpitations, and
hypertension. The increased workload on the heart can result
in myocardial infarction, essentially the heart working harder
than it can handle. Although rare, the stress placed on the
heart can also transiently weaken the musculature of the
heart to result in severe dysfunction, a condition known as
Takotsubo cardiomyopathy. Takotsubo cardiomyopathy is
still poorly understood but often mimics myocardial infarctions and presents with chest pain and hemodynamic instability, usually following extreme emotional or physical stress
and a sudden surge of catecholamines and corticosteroids.
Chronic stressful stimuli are also a well-described driver of
cardiovascular disease. High blood pressures and high volumes cause endothelial cell damage and are the driving force
behind atherosclerosis and vascular disease. These can lead
to coronary vascular disease and increased risk of myocar-
dial infarction, as well as microvasculopathies that can cause
renal disease and retinopathy, perfusion decits, and
impaired function of many organ systems. Overall, hypertension is the most important preventable risk factor for premature death worldwide [9].
Stress andtheImmune System
The immune system is signicantly altered in both acute and
chronic stress exposure. Whether or not these effects are proinammatory or anti-inammatory is variable depending on
the modality of stress, duration, repeated exposure, and an
individual’s perception of stress. The effect of chronic stress
on the function of the immune system is a major driver of
morbidity and mortality, so understanding the sequelae of
chronic stress is essential to maintaining health and resilience in those with high stress lifestyles and careers.
As is the case with the rest of the body, the immune system’s response to stressors begins with the HPA and SNS
response. These integrated neuroendocrine and autonomic
responses kick off signaling pathways that enhance humoral
immunity while suppressing cellular immunity. This switch
in modalities is accomplished by stimulating Th12 cells and
suppressing the function of Th1 and antigen presenting cells.
It is hypothesized that this is an evolutionary response to the
primary stressor of early humankind: infections. This shift
effectively limits the detrimental effects of a non-specic,
systemic immune reaction, while simultaneously enhancing
a specic, localized reaction. The proinammatory cytokines IL-1, TNFa, and IFNy are downregulated, while antiinammatory cytokines, IL-10, and TGFb are stimulated.
(Local tissues that are damaged or inamed can still attract
proinammatory cytokines via neutrophil recruitment.)
In contrast to this rapid response, long-term exposure to
stressful stimuli is a well-described risk for developing infection, autoimmune disease, and malignancy. This increased
incidence in disease is attributed to disruption in the homeostasis of defense mechanisms. Studies have shown that during acute stress, the concentration of CD16-rich NK cells
increases—which potentiate antibody-dependent immunity,
but chronic stress results in a decline in NK cytotoxic activity. Not only does the concentration of NKs decline with
chronic stress, but also their responsiveness to cytokines.
T-cells have also been shown to lose their proliferative
response to mitogens, lectins, and activation of the T-cell
receptor when exposed to chronic stress [10].
Cellular immunity isn’t the only thing affected by exposure to chronic stress. Several studies have demonstrated that
individuals suffering from chronic stress have a diminished
antibody response to vaccines. It is thought that chronic activation of the HPA axis leads to persistent elevation of glucocorticoids, which interrupts the normal balance of the Th1/
12 Biological andPsychological Interactions oftheStress Response: How toBuild Resilient Trauma Teams
75
Th2 response, thus hindering an appropriate response to vaccinations [11].
Failure to appropriately regulate the stress response in both
the SNS and HPA system have been linked to a variety of different pathologies. Hypertension, autoimmune disease, immunosuppression, affective, and psychological disorders have all
been described in relation to exposure to chronic stress. There
are well-described diagnoses like major depressive disorder
and PTSD that are directly related to stressful exposures. The
connection of chronic stress exposure and human disease is
still poorly understood and ongoing researching into prevention and therapy is of specic value to healthcare workers, rst
responders, military personnel, and other individuals regularly
exposed to high-stress situations [10].
The physiology and biochemical pathways involved in the
human stress response are complex and multifaceted. Not
every signaling pathway or secondary messenger translates
directly into the lived experience of an individual. First
responders, medical workers, and other members of trauma
teams need to be aware of the acute physical and behavioral
changes that accompany the stress response in order to recognize it and respond appropriately. This is important in the
acute setting to manage stress and be an effective operator in
each situation, but also in the setting of chronic sense to maintain resilience, health, and long-term performance (Fig.12.1).
Stress andSleep
During daily life, many of the body’s homeostatic mechanisms are maintained and regulated over a 24-hour period by
circadian rhythms, the body’s internal clock. Circadian
rhythms are maintained both by a neurological “masterclock” within the hypothalamic suprachiasmatic nucleus as
well as numerous autoregulatory peripheral feedback loops
in most tissues. Through a complex process of gene transcription, protein production, and negative feedback loops
on itself, the genes CLOCK and BMAL1 are able to generate
an internal 24-hour rhythm in the body, allowing for time-ofday-dependent maintenance and regulation of essential body
systems. Disruption of these internal mechanisms can lead to
suboptimal physiologic performance and response to stressors, thereby exacerbating the detrimental effects of acute and
chronic stress. Literature shows that disruptions to the normal maintenance of homeostasis through circadian mechanisms can manifest as cardiovascular, immune, metabolic,
and cognitive pathology. This is particularly important to
recognize for trauma teams, rst responders, and healthcare
workers, who are often subject to chaotic schedules and sudden interruptions at any time of the day.
Cortisol plays an important role in the maintenance of the
circadian rhythm, a physiologic pattern that promotes appropriate wakefulness and relaxation to optimize both performance and recovery. In humans, cortisol is secreted in an
anticipatory fashion, peaking in the morning just before
waking, followed by a steady decline until its lowest levels,
which are maintained during sleep. This system primes the
body for when it expects to be under the most stress, such as
during waking hours, and promotes relaxation when it is
time to sleep. Fluctuations in cortisol levels occur throughout
the day based on stressors and external factors, but the overall pattern of peak levels in the day time and lowest at night
is maintained solely by circadian mechanisms.
Cortisol levels are just one example of anticipatory
homeostatic control based on circadian rhythms. Tissue sensitivity to glucocorticoids, adrenal response to catecholamines, temperature control, and even behavior and physical
activity are all known to be dependent on the time of day.
Fig. 12.1 Simplied
schematic view of the human
stress response and major
downstream physiologic
effects. (Figure made with
BioRender)