The Journal of TRAUMA!
Injury, Infection, and Critical Care
Surgical Glue Grant
Inflammation and the Host Response to Injury, a Large-Scale Collaborative Project:
Patient-Oriented Research Core—Standard Operating Procedures for Clinical Care
III. Guidelines for Shock Resuscitation
Frederick A. Moore, MD, Bruce A. McKinley, PhD, Ernest E. Moore, MD, Avery B. Nathens, MD, PhD, MPH,
Michael West, MD, PhD, Michael B. Shapiro, MD, Paul Bankey, MD, PhD, Bradley Freeman, MD,
Brian G. Harbrecht, MD, Jeffrey L. Johnson, MD, Joseph P. Minei, MD, and Ronald V. Maier, MD
S
hock frequently accompanies severe trauma. In addi-
tion to acute mortality, shock is a predominant risk
factor for multiple organ dysfunction syndrome
(MODS) and shock resuscitation is an obligatory early inter-
vention. Because both under and over resuscitation contribute
to the pathogenesis of MODS, the potential for MODS de-
velopment can be minimized by developing a guideline to
insure early consistent and appropriate resuscitative efforts.
Submitted for publication January 20, 2006.
Accepted for publication April 19, 2006.
Copyright © 2006 by Lippincott Williams & Wilkins, Inc.
From the Department of Surgery (F.M., B.M.), University of Texas at
Houston; Department of Surgery (E.M., J.L.), University of Colorado; De-
partment of Surgery (A.N., R.M.), University of Washington; Department of
Surgery (M.W., M.S.), Northwestern University; Department of Surgery
(P.B.), University of Rochester; Department of Surgery (B.F.), Washington
University; Department of Surgery (B.H.), University of Pittsburgh; Depart-
ment of Surgery (J.M.), University of Texas at Southwestern; and the
Inflammation and the Host Response to Trauma Large Scale Collaborative
Research Program*
Supported by a Large-Scale Collaborative Project Award (U54-
GM62119) from The National Institute of General Medical Sciences, Na-
tional Institutes of Health
*Additional participating investigators in the Large Scale Collaborative
Research Agreement entitled, “Inflammation and the Host Response to
Trauma” include Henry V. Baker, PhD., Timothy R. Billiar, MD, Bernard H.
Brownstein, PhD, Steven E. Calvano, PhD, Irshad H. Chaudry, PhD, J.
Perren Cobb, MD, Chuck Cooper, MS, Ronald W. Davis, PhD, Adrian Fay,
PhD, Robert J. Feezor MD, Richard L. Gamelli, MD, Nicole S. Gibran, MD,
Doug Hayden, MS, David N. Herndon, MD, Jureta W. Horton, PhD, John
Lee Hunt, MD, Matthew Klein MD, Krzysztof Laudanski MD, MA, James
A. Lederer, PhD, Tanya Logvinenko, PhD, John A. Mannick, MD, Carol L.
Miller-Graziano, PhD, Michael Mindrinos, PhD, Lyle L. Moldawer, PhD,
Grant E. O’Keefe, MD, MPH, Laurence G. Rahme, PhD, Daniel G. Remick,
Jr. MD, David Schoenfeld, PhD, Robert L. Sheridan, MD, Geoffrey M.
Silver, MD, Richard D. Smith, PhD, Scott Somers, PhD, Ronald G. Tomp-
kins, MD, ScD. Mehmet Toner, PhD, H. Shaw Warren, MD, Steven E. Wolf,
MD, Wenzhong Xiao, PhD, Martin Yarmush, MD, PhD, Vernon R. Young,
PhD, ScD.
Address for reprints: Frederick A. Moore, MD, UTHSC – Houston
Medical School, Department of Surgery, 6431 Fannin Street, MSB 4.264,
Houston, TX 77030; e-mail: Frederick.A.Moore@uth.tmc.edu.
DOI: 10.1097/01.ta.0000225933.08478.65
82
J Trauma. 2006;61:82– 89.
The challenges of this guideline include: a) early identifica-
tion of high risk patients, b) implementation in environments
that are suboptimal for monitoring resuscitation, c) early
identification of resuscitation “non-responders” that require
more aggressive interventions, and d) avoiding potentially
harmful over zealous interventions.
This guideline is based on the best available evidence
and expert consensus discussions supported by the Inflam-
mation and Host Response to Injury Large Scale Collabora-
tive Project award from the National Institute of General
Medical Sciences, and is being used in the funded clinical
studies.1,2 The following section provides a brief overview of
the rationale for specific guideline recommendations. This is
followed by two algorithms that depict escalation in inter-
ventions and monitoring requirements in the subset of pa-
tients who do not respond to ongoing volume loading and/or
blood transfusions. With multi institutional experience and
critical analysis this resuscitation process may be further
refined; at this time it is intended to serve as a template for
interventional trials and to test the utility of new monitoring
technology. This protocol was designed for blunt trauma
patients who are presumed not to have a serious concomitant
brain injury. Its purpose is to guide resuscitation as soon as
feasible after arrival in the Emergency Department (ED) after
control of active torso bleeding.
Protocol Rationale
Early Recognition of Shock in the Emergency
Department
Recognizing the presence of shock and assessing its
severity are key factors in early identification of high risk
patients. Shock often can be detected by simple physical
examination findings in the ED resuscitation area. Dimin-
ished or absent peripheral (radial, pedal) or central (carotid,
femoral) pulses, decreased capillary refill associated with
pallor or cool clammy extremities may all denote the pres-
ence of shock and hypovolemia. The initial blood pressure
(BP) measurement should be performed using a manual cuff
because automatic cuff BP measurement devices may over-
July 2006

estimate systolic BP (SBP) in hypovolemic trauma patients.3
A SBP ! 90 mm Hg and/or a heart rate (HR) " 130 bpm is
generally considered to be indicative of shock. Some patients
(especially the young) compensate for hypovolemia and
maintain a normal SBP even in the face of significant ongo-
ing hemorrhage although this is often associated with tachy-
cardia. Additionally, because acute massive blood loss may
paradoxically trigger a vagal-mediated bradycardia, the tra-
ditional inverse correlation between increased HR and de-
creased effective blood volume may not hold in the early
resuscitation period.4 The initial hemoglobin concentration
([Hb]) is notoriously misleading because there has not been
sufficient time for influx of interstitial fluid into the intravas-
cular space and the patient has not yet been volume resusci-
tated. Therefore, it is important to measure the [Hb] again
after the initial 2 L of crystalloid loading, a decrease greater
than 2 g/dL is grounds for concern. The magnitude of arterial
base deficit (BD) has been shown to be a useful index of the
severity of hemorrhagic shock. A BD ! 6 mEq/L is indica-
tive of severe shock.5 Serial BD determinations are important
in determining the effectiveness of interventions and lack of
response is indicative of a poor prognosis. Other less well
studied markers of the severity of shock include venous blood
lactate, bicarbonate concentrations and end-tidal CO2 to
PaCO2 differences.
Volume Loading With Isotonic Crystalloid Fluid
The key step in resuscitation of the injured patient is the
control of active hemorrhage. The actively bleeding patient
cannot be adequately resuscitated without hemorrhage con-
trol. Resuscitation with isotonic crystalloid fluids has been
the standard of care in the United States since the late l960s.
The laboratory work of Shires and Moyer demonstrated the
best survival was achieved with large volume isotonic crys-
talloid solution. The basic concept is that interstitial fluid
moves into both the intravascular and intracellular spaces in
response to shock and that adequate resuscitation requires
replenishment of both the intravascular and interstitial spaces.
Their studies demonstrated that the optimal ratio of isotonic
crystalloid infusion to shed blood infusion was 3 to 1. Sub-
sequent studies demonstrated that the optimal ratio for sur-
vival after severe shock increases and can be as high as 8 to
1.6,7 Clinical trials were performed in the l970s and 1980s
that compared isotonic resuscitation and colloid resuscitation.
Individually, these trials were underpowered and reported
conflicting results. When subjected to meta-analysis, they
have yielded no consistent differences in overall outcome.
When the same data were subjected to subgroup analysis,
however, the use of isotonic crystalloids in trauma patients
was associated with improved survival. A large clinical trial
published in 2004 found no differences in outcome between
crystalloid and colloid resuscitation in ICU patients, but
again, subgroup analysis demonstrated improved outcomes in
trauma patients receiving crystalloid.8 Although these sub-
group analyses are not definitive, they are consistent with the
Volume 61 • Number 1
Guidelines for Shock Resuscitation
early laboratory studies, which indicated that survival in
hemorrhagic shock is improved with large volume crystalloid
resuscitation. However, in recent years, “damage control”
surgery combined with prompt ICU resuscitation appears to
be salvaging more patients who are arriving with exsangui-
nating hemorrhage. Unfortunately, over zealous crystalloid
infusion appears to have adverse consequences, e.g. cerebral
edema (increased ICP), acute lung injury (worsened pulmo-
nary edema), and the abdominal compartment syndrome (pri-
mary and secondary).9
Lactated Ringer’s is the Preferred Isotonic
Crystalloid
Although newer formulations (e.g. Ringer’s ethyl pyru-
vate) are being tested clinically, normal saline (NS) and
lactated Ringer’s (LR) remain the most commonly used iso-
tonic fluids. In theory, LR is preferable to NS because it
provides a better buffer for metabolic acidosis, but to date,
investigators have not documented any important differences
in outcome. Moreover, the D isomer of lactate may have
adverse immunoinflammatory properties. One laboratory
study found that NS and LR were equivalent in the setting of
moderate hemorrhagic shock but that in the setting of massive
hemorrhage, NS was associated with greater physiologic de-
rangement (e.g. hyperchloremic acidosis) and a higher
mortality.10 Clinical experience confirms the adverse effects
of iatrogenic hyperchloremic acidosis. In addition, the poten-
tial benefits of using hypertonic saline (HTS) – rapid blood
pressure response, decrease in ICP and improved immuno-
logic status – for resuscitation are unproven but currently in
clinical trials.
Blood Transfusion to Maintain Hemoglobin
Concentration at 10 g/dL
The optimal [Hb] continues to be a subject of intense
debate. Early laboratory studies of shock resuscitation sug-
gested that survival was improved when [Hb] was maintained
in the range of 12 to 13 g/dL. Subsequent studies using
isovolemic hemodilution models indicated that the optimal
[Hb] for maintaining oxygen delivery was 10 g/dL, and, until
relatively recently, this value was the recommended level for
critically ill patients. Currently, there is a growing recognition
that administration of stored packed red blood cells (PRBC)
can adversely affect outcome by modulating the inflamma-
tory response (by both amplifying early proinflammation and
aggravating late immunosuppression) and by impairing tissue
perfusion (limiting access to or obstructing the microcircula-
tion as a consequence of decreased RBC deformability). A
1999 randomized trial found that patients who received trans-
fusions according to a restrictive policy (i.e. transfusion when
the [Hb] fell below 7 g/dL) did as well as, and possibly better
than, patients who received transfusions on a more liberal
basis (i.e. transfusion when [Hb] fell below 10 g/dL).11 How-
ever, this study was done in a select group of euvolemic
patients in which those with active hemorrhage were ex-
83
 The Journal of TRAUMA! Injury, Infection, and Critical Care
cluded; thus, it is not applicable to severely injured trauma
patients requiring active shock resuscitation, but is cogent as
their clinical course progresses. (See SOP for blood transfu-
sions.) In addition, if blood transfusions are to be restricted
during active resuscitation, it is not clear which alternative
fluids should be used. Colloid solutions have been associated
with complications and indiscriminant use of crystalloid fluid
is detrimental.9 Hypertonic saline and hemoglobin based ox-
ygen carriers are attractive alternatives, but additional clinical
trials are needed before these could become standard of care.
Additionally, maintaining higher [Hb] during active bleeding
may facilitate coagulation. Many patients who are resusci-
tated by this process will also require a massive transfusion
(i.e. "10 units PRBC in 24 hour), and are at risk for devel-
oping a coagulopathy. This subset of patients may benefit
from early fresh frozen plasma (FFP) administration and this
should be factored into their volume loading regimen.
Early Central Venous Pressure Monitoring
The most likely etiology of shock following major
trauma is hypovolemia secondary to acute blood loss. There-
fore, initial volume loading with isotonic crystalloids (1 L
boluses in adults and 20 cc/kg in children) is recommended.
The response to this empiric volume loading assists in early
triage decisions. Prompt correction of abnormal vital signs
indicates that a lesser volume deficit (10 –20% blood volume)
was present and that an expedited trauma evaluation can be
safely performed to rule out occult bleeding. Patients who do
not respond to empiric volume loading may have severe
hypovolemia (30 – 40% blood volume), cardiogenic shock or
neurogenic shock. Given that neurogenic shock is usually
well tolerated and typically responds to initial volume load-
ing, the key issue is to quickly distinguish hypovolemic shock
from cardiogenic shock. Placement of a catheter that permits
reliable measurement of central venous pressure (CVP) fol-
lowing the initial boluses can help differentiate these states. A
high CVP ("15 mm Hg) suggests cardiogenic shock (likely
etiologies include tension pneumothorax, pericardial tampon-
ade or myocardial contusion/infarction). A low CVP (!5
mm Hg) may indicate acute ongoing blood loss, and man-
dates focus on identifying occult sources of blood loss. In
many instances control of hemorrhage requires operating
room (OR) or interventional radiologic (IR) interventions.
Patients who initially respond to volume loading, but require
ongoing crystalloid volume and/or blood transfusion during
expedited trauma evaluation, or who have evidence of severe
shock by ABG (i.e. BD ! 6 mEq/L), should have a central
venous line placed and have continuous CVP measurements
displayed to assist with ongoing resuscitation until the pa-
tients arrives in the intensive care unit (ICU). In the ICU, with
more intensive monitoring available, the decision needs to be
made if escalation to pulmonary artery (PA) catheterization is
warranted.
84
Pulmonary Artery Catheterization in the ICU
The primary goal of shock resuscitation is the early
establishment of “adequate” oxygen delivery (DO2) to vital
organs. The yet to be resolved controversy is what is “ade-
quate.” The calculated variable DO2 is the product of cardiac
output (CO) and arterial oxygen content (CaO2). By conven-
tion, CO is indexed to body surface area and expressed as
cardiac index (CI), and when multiplied by CaO2 yields an
oxygen delivery index (DO2I). Normal DO2I is roughly 450
mL/min/m2. CaO2 and DO2I are calculated as follows:
CaO2 (mL O2/dL) # [Hb] (g/dL) x 1.38 mL O2/g Hb x
SaO2 (%) $ [PaO2 (mmHg) x 0.003 mL O2/mmHg]
DO2I (mL/min/m2) # CI (L/min/m2) x CaO2 (mL/dL) x
10 dL/L,
where [Hb] is hemoglobin concentration, SaO2 is hemoglobin
O2 saturation, PaO2 is arterial oxygen tension, and 0.003 is
solubility of O2 in blood. Thus, there are four variables (i.e.
PaO2, SaO2, [Hb], and CI) that determine DO2I. Of the four
variables CI is the most difficult to monitor and manipulate.
This is the rationale for liberal use of the PA catheter in
severely injured patients. Myocardial dysfunction during
traumatic shock resuscitation is common, but usually re-
sponds to volume loading. However, once a patient has been
volume loaded (CVP "15 mm Hg) and has evidence of
ongoing shock (e.g. decreased MAP, increased BD or lactate
levels), a PA catheter is warranted to better monitor cardio-
vascular function, especially filling pressures and CI. Once
the PA catheter is placed, the key question is what CI is
acceptable. Early work from Shoemaker et al. demonstrated
that the “survivor” response to traumatic stress is to become
hyperdynamic (CI " 4.5 L/min/m2) and consequently have
supranormal DO2I ("600 mL/min/m2).12 Supranormal DO2I
was, therefore, proposed to be the resuscitation goal. Subse-
quent prospective randomized controlled trials (RCTs), how-
ever, failed to demonstrate improved outcome with goal ori-
entated resuscitation to supranormal DO2I. In fact, several
recent studies indicate that this strategy is harmful.13 Recent
studies in which a normal DO2I goal of 500 mL/min/m2 was
used demonstrated that patients achieve similar hyperdy-
namic responses to standardized interventions, require less
volume loading, and have better outcomes than patients re-
suscitated to a supranormal DO2I goal.14,15 We recommend
using a CI ! 3.8 L/min/m2 as the resuscitation goal for this
resuscitation process guideline. During active resuscitation,
most severely injured patients will have SaO2 " 92% and
[Hb] " 10 g/dL and, therefore, DO2I will approach 500
mL/min/m2. PA catheters capable of continuous monitoring
of CO and mixed venous hemoglobin oxygen saturation
(SmvO2) are now commonly available and should be utilized.
These continuously monitored variables provide rapid feed-
back that is often necessary to guide effective, timely resus-
citation interventions. This approach is based on expert opin-
ion as there are no data to suggest that a PA catheter is either
July 2006

Table 1 Vasoactive Agents Commonly Used in Shock Resuscitation
Agent Dose Rate ("g/kg/min) Physiologic Action
Dopamine
Low !5 DA1 receptor
Medium 5–15 #1 receptor
High " 15 $1 receptor
Dobutamine 5–20 $1, #1, #2
receptors
Norepinephrine 0.01–0.05 $1, #1 receptors
" 0.05 $1 receptor
Nitroprusside 0.25–10 NO donor
Phenylephrine 0.2–0.9 $1 receptor
Vasopressin 0.04 units/min Vasopressin
receptor
$ 1, post synaptic receptor on vascular smooth muscle; $ 2-pre synaptic receptor; # 1, largely cardiac; # 2, largely smooth muscle receptor
of vasculature and bronchial tree; DA1, dopaminergic post synaptic receptors in renal, splanchnic, cerebral and coronary vessels; CO, cardiac
output; MAP, mean arterial pressure; PCWP, pulmonary capillary wedge pressure; HR, heart rate
harmful or beneficial in severely injured patients undergoing
shock resuscitation.
Assessment of Pre-Load by PCWP and the use of the
“Starling Curve” Intervention
The traditional variable used to assess volume status is
the pulmonary capillary wedge pressure (PCWP). It is
important to recognize that significant hypovolemia can
exist despite reasonable PCWP. Peripheral vasoconstric-
tion of less acutely essential organs (e.g. kidney, gut,
muscle, and skin) results in blood volume shifts to main-
tain the central circulation and perfusion of more essential
organs (e.g. heart and brain). With a low CI and a low
PCWP (i.e. !10 mm Hg), volume loading should be un-
dertaken. After the PCWP increases to !15 mm Hg, the
benefits of increasing CI by the Frank Starling mechanism
should be considered. If additional CI is needed then a
stepwise incremental volume loading intervention is used
to identify the optimal CI-PCWP “operating point.” Be-
cause the shape and position of the Frank Starling curve is
dependent on left ventricular contractility, compliance and
afterload, it is difficult to identify optimal or plateau
PCWP during volume loading without frequent sequential
measurements.16 In a recent study, one-third of high risk
patients had persistently low CO, high systemic vascular
resistance (SVR) and high BD despite volume loading to a
PCWP ! 15 mm Hg. However, these patients did respond
well to the “Starling curve” intervention, by increasing
CO, decreasing SVR and decreasing BD. This observation
is consistent with a recent RCT in which patients who did
not respond to initial volume loading (to presumed euvol-
emia) were randomized to additional volume loading or to
a vasodilating inotropic agent.17 Patients who received
further volume loading were found to have a better resus-
citation response than those treated with inotropic agents.
This favorable response to additional pre-load must, how-
ever, be weighed against the risks of increasing hydrostatic
pressure leading to increase pulmonary edema, especially
Volume 61 • Number 1
Guidelines for Shock Resuscitation
Intended Effects Adverse Effects
selective vasodilation 1 HR
1 CI, 1 MAP, 1 PCWP Arrhythmia
1 MAP
1 CI, 2 PCWP 1 HR, 2 MAP, arrhythmia
1 CI 1 afterload
1 MAP Vasoconstriction
2 afterload, 1 CI 2 MAP, 2 PaO2 thiocyanate toxicity
1 MAP Vasoconstriction
1 MAP Vasoconstriction
in patients with leaky endothelium (e.g. pulmonary contu-
sion). Increasing PCWP "25 mm Hg in attempts to create
a “Starling curve” should not be done because of the
potential of causing or worsening pulmonary edema.16
Use of Vasoactive Agents in Non-Responders
The primary early problem in shock resuscitation is
decreased preload with resulting decreased CO. In this
setting, the normal “survivor” response is to become hy-
perdynamic with volume loading. However, as time and
severity of shock increases, a complex pathophysiologic
interaction evolves that limits CO. Important factors in-
clude relative hypovolemia, primary or secondary myocar-
dial dysfunction and excessive peripheral vasoconstriction.
With ineffective intervention, shock will ultimately
progress into pathologic vasodilation which heralds irre-
versible shock. Unfortunately, in the later phases of shock,
patients who do not respond to volume loading also do not
consistently respond to vasoactive agents. Therefore, a PA
catheter should be placed to more accurately characterize
their hemodynamic profile and monitor their response to
vasoactive agent administration. A specific agent with
known physiologic actions should then be administered
and titrated to a desired effect. (See Table 1.)
For the typical non responding patient (i.e. low CI,
adequate PCWP and high SVR), a vasodilating inotrope
such as dobutamine (beware of hypotension) or dopamine
(beware of tachycardia) is recommended. Patients with a
particularly high SVR may respond better to simple after-
load reduction with nitroprusside. However, additional
volume loading may be needed to maintain an adequate
PCWP and oxygenation may worsen due to loss of hypoxic
pulmonary vasoconstriction (i.e. worsened V/Q mis-
match). For patients with low CO and normal SVR, dopa-
mine or lower dose norepinephrine are reasonable choices.
For patients who have low SVR and are thus unable to
maintain an adequate MAP (! 60 mm Hg), higher doses of
norepinephrine should be used. It is also important to rule
85
 The Journal of TRAUMA! Injury, Infection, and Critical Care
Fig. 1. Initial resuscitation.
out relative adrenal insufficiency in patients requiring
higher doses of norepinephrine.18 Additionally, low dose
vasopressin (as replacement therapy) may reduce the need
for norepinephrine in patients exhibiting impending irre-
versible shock.19 Of note, there are no data that demon-
strate that use of a specific vasoactive agent in non-re-
sponding patients improves outcome. Several studies have
demonstrated improved hemodynamic responses to spe-
cific agents, and extrapolate this response to an improved
outcome.20 –22
Protocol Summary
Initial Resuscitation
Figure 1 depicts initial ED resuscitation and the follow-
ing text includes explanatory annotations lettered A through
F. Variables that drive decision making include SBP, HR,
BD, [Hb], CVP and clinical judgment (ever present). Addi-
tionally, stopping ongoing active hemorrhage is paramount to
the survival of these patients.
A. Major trauma patients arriving in shock (SPB !90 mm
Hg and/or HR "130 bpm) are initially managed by using
Advanced Trauma Life Support (ATLS).22 Routine mon-
itoring includes frequent vital signs (minimum q 15 min-
utes), continuous ECG and pulse oximetry (SpO2) and
core body temperature. A data flow sheet is necessary to
trend physiologic indices, laboratory test results and fluid
volume/blood transfusion administration. During the ini-
tial ED evaluation an ABG analysis should be obtained in
all patients presenting in traumatic shock.
B. Major torso trauma patients who have evidence of shock
(documented by early SBP !90 mm Hg and/or a BD !6
mEq/L), and who require ongoing resuscitation, should
have a central venous line (via subclavian or internal
jugular vein) placed in ED. CVP measurements should be
86
used to differentiate the type of shock and to assist with
subsequent monitoring of shock resuscitation.
C. Early CVP "15 cm mmHg (before extensive volume
loading) suggests cardiogenic shock.
D. Differential diagnosis of cardiogenic shock following
blunt trauma includes: 1) tension pneumothorax, 2) myo-
cardial contusion/infarction, 3) pericardial tamponade
(uncommon) and 4) air embolus (rare). Specific diagnosis
and treatment is beyond the scope of this protocol. ATLS
guidelines should be followed.23
E. CVP !10 mm Hg despite volume loading indicates per-
sistent hypovolemia and this most likely reflects ongoing
bleeding. The endpoint of initial resuscitation is contro-
versial and the algorithm statement “resuscitate until sta-
ble” is intentionally vague (i.e. requires clinical judg-
ment). The crux of the issue is whether it is preferable to
administer fluids to restore DO2 to the vital organs (risk-
ing hemodilution and disruption of early hemostatic clots)
or to withhold fluid resuscitation until control of hemor-
rhage (risking prolonged cellular shock to the extent that
it becomes irreversible by the time hemorrhage control is
accomplished). At present, the rationale compromise is
hypotensive resuscitation (SBP "90 mm Hg and HR
!130 bpm) with moderate volume loading until hemor-
rhage control is accomplished. This approach is becoming
the standard of care for penetrating trauma victims. It is
most likely safe for blunt torso trauma patients who do not
have significant concomitant brain injuries that could be
worsened by permissive hypotension.
F. LR boluses should continue and, when LR infusion ex-
ceeds 30 mL/kg, blood should be administered. Earlier
empiric blood transfusion is indicated in patients (espe-
cially the elderly) who arrive in severe shock or who have
injuries associated with significant bleeding (e.g. vertical
July 2006

Fig. 2. ICU resuscitation.
shear pelvic fracture or bilateral femur fracture.) Protocols
for massive transfusion should be established with the
blood bank to ensure prompt availability of blood prod-
ucts for patients arriving with ongoing life-threatening
hemorrhage. Among the most devastating complications
of massive blood and fluid administration is a coagulopa-
thy. Stored blood is deficient in factors V and VIII and
platelets. Timely administration of FFP and platelets will
minimize risk of coagulopathy after massive transfusion.
Presumptive factor replacement is usually not indicated in
the early phase of resuscitation, but may be appropriate in
patients with massive hemorrhage caused by significant
intracavitary bleeding or an unstable pelvic fracture.24,25
ICU Resuscitation
Hemorrhage control is of paramount importance in the
initial management of major torso trauma patients arriving
in shock. It is assumed that this issue will have been
addressed in the vast majority of patients by the time the
patient is admitted to the ICU. The priorities in early ICU
care are to: a) optimize resuscitation, b) correct hypother-
mia, coagulopathy and acidosis and c) monitor for ongoing
bleeding requiring OR or IR intervention. Figure 2 depicts
ICU resuscitation and the following text includes explan-
atory annotations lettered A through H. An important early
Volume 61 • Number 1
Guidelines for Shock Resuscitation
decision is whether to escalate monitoring interventions
(i.e. placement of arterial and PA catheters). Variables that
drive decisions in the PA catheter algorithm include CI,
[Hb], PCWP, BD and clinical judgment.
A. When the patient arrives in the ICU, the physician
needs to decide whether to continue resuscitation using
serial vital signs, CVP, [Hb] and BD determinations
(i.e. CVP Algorithm.) Most patients can be managed
using this process, but close observation by a physician
at bedside is required because CVP is a very indirect
monitor of hemodynamic function.
B. For patients who are not responding to ongoing volume
loading/blood transfusion (i.e. low MAP or persistently
high BD) and/or are demonstrating secondary organ
dysfunctions (i.e. worsening oxygenation or decreased
urine output), pulmonary artery catheterization is war-
ranted. The possibility of an impending abdominal
compartment syndrome needs to be considered if crys-
talloid fluid volume loading exceeds 10 L or PRBC
transfusion exceeds 10 units. Periodic urinary bladder
pressure measurements should be obtained to monitor
for onset of abdominal compartment syndrome. Uri-
nary bladder pressure !25 mm Hg indicates significant
abdominal hypertension and need for bedside assess-
ment for possible surgical intervention.9,14
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 The Journal of TRAUMA! Injury, Infection, and Critical Care
C. It is assumed that most patients being treated by this
algorithm will be intubated. If not intubated and requiring
ongoing volume loading, intubation needs to be consid-
ered, because worsening pulmonary function is likely. If
intubated and PEEP !12 cm H2O, the effects of high
mean airway pressures on cardiac function needs to be
considered, as does use of PA catheter.
D. If the patient meets the CI goal of 3.8 L/min/m2, then the
patient should be monitored as depicted in this arm of algo-
rithm. Hemodynamic variables should be assessed hourly,
and possibly more frequently. Laboratory variables includ-
ing [Hb] and ABG (BD) should be determined every 4
hours, and possibly more frequently until the patient is fully
resuscitated and stable. Coagulation variables and urinary
bladder pressure measurements should be monitored as
deemed necessary.
E. Most young patients easily exceed the CI goal of 3.8
L/min/m2 with modest crystalloid volume loading and
blood transfusion. There is no need to increase PCWP
to high levels in responding patients, but [Hb] should
be maintained !10 g/dL during acute resuscitation to
assure a safety margin in the event of occult or recur-
ring bleeding. However, once the BD has been normal-
ized and the need for ongoing volume loading has
resolved, a lower [Hb] is acceptable. (See SOP for
transfusion.)
F. PCWP may not accurately reflect left ventricular end
diastolic volume and increasing PCWP to !15 mm Hg
may enhance cardiac performance. The optimal rela-
tionship between PCWP and CI can be determined by
incrementally increasing left ventricular preload
(PCWP) and then measuring cardiac output (CI) in
response, i.e. by generating a “Starling curve” to deter-
mine the optimal CI-PCWP operating point.10 This
should only be done in patients who are not meeting the
CI goal and who have evidence of ongoing shock (i.e.
persistently elevated BD.)
G. After obtaining optimal PCWP, if CI !3.8 L/min/m2,
then infusion of a vasodilating inotropic agent should
be started. Dobutamine is recommended as the pre-
ferred inotropic agent. Dobutamine infusion should be
started at a dose rate of 5.0 "g/kg/min and increased in
increments of 2.5 "g/kg/min to a maximum of 20
"g/kg/min to increase CI. If the patient does not tol-
erate the vasodilation, dopamine should be considered
with progression from low to mid- to high dose, while
monitoring for excessive tachycardia.
H. Occasionally, an inotropic agent with vasoconstrictive
effects may be needed to maintain MAP !60 mm Hg,
enhance myocardial contractility and maintain coro-
nary perfusion pressure. These agents decrease periph-
eral perfusion at the microcirculatory level by $1 va-
soconstriction of metarterioles thereby prolonging or
exacerbating the effects of shock, and are therefore an
intervention of last resort. Norepinephrine is recom-
88
mended as the preferred agent. Norepinephrine infu-
sion should be started at 0.05 "g/kg/min and increased
in increments of 0.05 "g/kg/min as needed to obtain CI
!3.8 L/min/m2, and maintain MAP !60 mm Hg. The
maximum recommended norepinephrine dose rate is
0.2 "g/kg/min. Adrenal insufficiency in patients re-
quiring norepinephrine to maintain MAP needs to be
ruled out. Low dose vasopressin may decrease the
required dose of norepinephrine.
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