1. health and fitness
2. disease

v ^ S ^ r r p ^ 2-19
CONTINUING EDUCATION
© 2005 Uppineott Williams & Wilkins, Itic,
Hypovolemic Shock
An Overview
Dorothy M. Kelley, MSN, RN, CEN
Resuscitation of major trauma victims suffering from shock remains a challenge for trauma systems
and trauma centers. Rapid identification, and ensuring correct, aggressive treatment, are necessary
for patient survival. This article discusses shock encountered in trauma victims: hypovolemic, cardiogenic, obstructive, and distributive shock. Emphasis is placed on hypovolemic shock and its
sequelae. The critical care nurse plays an important role as part of the team involved in the resuscitation and ongoing care of these patients. Understanding the underlying pathophysiology,
recognizing signs and symptoms, and being prepared to effectively respond will further enable
the nurse to contribute to positive patient outcomes. Key words: hypovolemia, resuscitation,
shock, trauma
R
ESUSCITATION of major trauma victims
suffering from shock remains a challenge for trauma systems and trauma centers. Rapid identification, and ensuring correct, aggressive treatment, are necessary for
patient survival. Trauma patients are at risk
for several types of shock states: hypovolemic, cardiogenic, obstructive, and distributive. Physiologically, regardless of the type of
shock, inadequate tissue perfusion is the result of reduced or poorly distributed blood
volume. The body activates compensatory
mechanisms in an effort to improve perfusion. Care providers must recognize and intervenerapidlyto support tissue oxygenation
and blood flow; otherwise, these compensatory mechanisms will fail, resulting in a cascade of events to include inflammatory response, release of mediators, organ failure,
and death.'
The critical care nurse plays an important
role as part ofthe team involved in the resuscitation and ongoing care of these patients. Understanding the underlying pathophysiology,
recognizing signs and symptoms, and being
prepared to effectively respond will further
enable the nurse to contribute to positive patient outcomes.
This article describes these 4 categories
of shock states. However, since hypovolemic
shock is the most common type of shock
encountered in the trauma patient population, the majority of the discussion will be
dedicated to its recognition, definition, and
treatment.
CASE STUDY
A 35-year-old male, helmeted motorcycle
driver, "T-boned" a taxicab at high speed. He was
ejected, landing on pavement 30 ft from his bike.
Witnesses accessed the 911 emergency medical response system; paramedics arrived quickly.
They found the patient lying unresponsive on the
pavement; respirations were agonal; pulse, weak,
and thready; BP was unobtainable. They placed
the patient in full spinal immobilization, administered oxygen, and supported respirations via a
bag, valve, mask (BVM) device. Transport time
was less than 2 minutes from the trauma center,
so they elected to "scoop and haul." Upon arrival,
the trauma team evaluated the patient, using Advanced Trauma Life Support (ATLS) guidelines
and reported these findings upon primary survey:
Ainway: patent; C spine precautions maintained
Breathing: No spontaneous respirations
Corresponding author: Dorothy M. Kelley, MSN, RN, CEN, Circulation: Thready femoral pulse rate 56;
11076 Montaubon Way, San Diego, CA 92131 (e-mail: hypotensive with unobtainable blood pressure.
kelley. dorothy®scrippshealth. org).
Skin, cool pale and dry.
From the Scripps Mercy Hospital, San Diego, Calif.
Hypovolemic Shock
Disability: GCS 3, pupils unequal, slightly
reactive.
The patient was intubated immediately upon arrival, using rapid sequence intubation (RSI) technique. Breath sounds auscultated after Intubation
was diminished, despite validation that the ET
tube was correctly placed. The respiratory therapist reported difficulty ventilating the patient. Bilateral needle thoracostomy was performed. A right
femoral vein cordis was placed, as well as insertion of 2, large bore, 16-gauge, peripheral intravenous catheters, A clot was sent off for type and
cross. Normal saline solutions were administered
intravenously; the patient remained hypotensive
and bradycardic. On secondary survey the patient was found to have the following:
Head: abrasions and scalp laceration with occipital skull fracture
Chest: diminished breath sounds; CXR, negative for hemothorax
Abdomen: multiple contusions, distended, hypoactive bowel sounds
Pelvis: unstable to compression and palpation
GU: absent rectal tone (paralytics on board
from RSI); meatus WNL; prostate WNL
Extremities: dusky, delayed capillary refill, unable to palpate peripheral pulses
Back/spine: no obvious step off
A foley catheter was inserted. Focused Abdominal Sonogram for Trauma (FAST) was negative. Blood for baseline laboratory studies was
sent off, and radiological studies were ordered
Laboratory findings: ABG, pH 7.01; PCO2 68;
P02 38; BE - 1 3 ; HCO3 11.7%; OzSat 59%; O2
15L/min 100%; INR 1.5.
The patient remained hypotensive. Pulse varied widely between a low of 32 and high of 120.
After infusion of warmed crystalloid, packed red
blood cells and FFP the BP stabilized at 102 systolic. Cardiac monitor demonstrated regular sinus rhythm at 98. The trauma surgeon elected
to transport the patient, with the trauma team in
attendance, to radiology for CT scan.
CT results: Closed head injury with intraparenchymal contusions; C-spine fractures at
multiple levels; T-spine fractures; open book
pelvic fracture, with intrapelvic blood vessel injuries, multiple lower extremity fractures.
matic" shock. Initially, he suffered from obstructive shock as a result of tension pneumothorax. Further investigation revealed that
the patient suffered from hypovolemic shock
from pelvic fractures and internal injuries. He
had also suffered distributive shock secondary
to cervical and thoracic cord transection associated with spinal column fractures. His lifethreatening, multisystem injuries proved challenging to sort out. However, hypovolemic
shock must always be the primary consideration until ruled out.
The case described above demonstrates the
complex critical thinking processes required
by trauma team members. This patient exhibited classic signs and symptoms of "trau-
ROLE OF TRAUMA CENTERS
TRIMODAL DEATH PATTERN
Researchers have identified 3 major epidemiological events, or trimodal patterns of
death from trauma. Immediate deaths, those
that occur on scene shortly after injury, account for approximately 50% of deaths due
to trauma. These usually result from cataclysmic events resulting in high central nervous system injuries, or devastating injuries
such as lacerations to the heart or major
blood vessels. Early deaths occur within several hours and are typically the sequelae of
acute hemorrhage or traumatic brain injury.
Late deaths may occur weeks after injury and
are typically the result of infection or multisystem organ failure. The preponderance of data
demonstrates that immediate and early deaths
account for approximately 80% of traumarelated fatalities, with the majority as a result of rapid exsanguination. There is a preventable death rate associated with a failure to
recognize and adequately treat patients at risk
for acute hemorrhage. This has been reported
as high as 27%. These data suggest that the
development and implementation of a strategic approach to provide care for at-risk patients could greatly improve outcomes. Goals
are aimed at early recognition, and adequate,
timely treatment to reduce the overall death
rate.^
Trauma systems have been designed to get
the "right patient, to the right resources, in
4
CRITICAL CARE NURSING QUARTERLY/JAMJARY-MARCH
the right time frame." Inclusive trauma systems assure the availability of rapid transport,
by adequately trained prehospital providers,
to centers prepared to receive the critically injured patients. The "right resources" and destinations are typically trauma centers, which
are required to demonstrate rigorous physical plant and care provider requirements. The
right time frame is sometimes referred to as
the "golden hour."' The cornerstone of this
approach is the rapid recognition and early
evaluation and treatment of severely injured
patients.^ This early resuscitation phase has
typically taken place in emergency departments; however, the resuscitation phase has
now moved beyond the walls of the emergency department and now includes operating room resuscitation and continued aggressive resuscitation in the intensive care unit
GCU). Therefore it is imperative that nurses in
these arenas be proficient In the recognition,
assessment, and care of the severely injured
trauma patient.'
DEFINITION
As described in the literature, there are
multiple definitions of shock. In the 1870s,
Samuel D. Gross described shock as the "rude
unhinging of the machinery of life."^ One
hundred years later, in the 1970s, G. T. Shires
discussed the severity of shock states as proportional to the depression in the cellular
membrane potential. He proposed that shock
occurs when the physiologically regulated circulation of blood fails to deliver sufficient oxygen to sustain aerobic metabolism to the cellular mitochondria. Therefore, resuscitation
from shock is restoration of adequate oxygen deUvery to mitochondria. Organ failure,
as shock sequelae, is proportional to the hypoxic damage to intrinsic cellular function.'
As defined by Advanced Trauma life Support
(ATLS), shock is the consequence of insufficient tissue perfusion, resulting in inadequate cellular oxygenation and an accumulation of metabolic waste. The consequences of
untreated shock are metabolic derangements
that result in a vicious cascade to include hy-
2005
pothermia, acidosis, and coagulopathy. If unresolved, shock progresses to an irreversible
state, resulting in multisystem organ failure
and death.^ Others have further described
shock as a basic biochemical inability to properly utilize oxygen and other nutrients, or an
inappropriate or ampMed stimulation of cellular signaling cascades.^
SHOCK CLASSIFICATIONS
Although there are a variety of definitions
and methods of classification,^"^ for the purposes of this discussion, shock is divided
into 4 pathophysiologic categories: (1) hypovolemic, (2) obstructive, (3) cardiogenic, and
(4) distributive. All the 4 interfere with endorgan cellular metabolism.^-*°
HYPOVOLEMIC SHOCK
Hypovolemic shock occurs as a result of decreased circulating blood volume, most commonly from acute hemorrhage. It may also be
the result of fluid sequestration w^ithin the
abdominal viscera or peritoneal cavity. The
severity of hypovolemic shock depends not
only on the volume deficit loss, the time frame
within which the fluid is lost, but also on the
age and preinjury health status of the individual. Clinically, hypovolemic shock is classified
as mild, moderate, or severe, depending on
the whole blood volume loss.'"
In mild or compensated shock, less than
20% of blood volume is lost. Vasoconstriction begins and redistribution of blood flow
is shunted to critical organs. Moderate shock
reflects 20% to 40% of blood volume loss;
there is decreased perfusion of organs such
as kidneys, spleen, and pancreas. In severe
shock, greater than 40% of blood volume is
lost; there is decreased perfusion of the brain
and heart. Hypovolemic shock produces compensatory physiologic responses in almost all
organ systems. 10
Pathophysiology of hypovolemic shock
Hypovolemic shock usually means hemorrhagic shock in the trauma patient. The
Hypovolemic Shock
patient may be bleeding internally or externally, and as a result circulating blood volume is decreased. This volume loss reduces
both preload and stroke volume and causes
reduced cardiac output.
Signs and symptoms of early hypovolemic
shock include an altered level of consciousness, sometimes manifested in agitation and
restlessness, or any central nervous system
depression. Physical assessment may demonstrate nonspecific signs and symptoms such as
cool, clammy skin, orthostatic hypotension,
mild tachycardia, and vasoconstriction.'' The
body is able to sustain blood pressure and
tissue perfusion by employing compensatory
mechanisms that primarily promote vasoconstriction to support an increase in intravascular volume,^
Late signs of shock include worsening
changes in mental status to include coma, hypotension, and marked tachycardia. It is important to know, however, that healthy adults
with impending hemorrhagic hypovolemic
shock may not become hypotensive untU as
much as 30% of their circulating blood volume
is lost."
VASOCONSTRICTION
Vasoconstriction is an early compensatory
response mechanism to shock. The initial decrease in blood pressure inhibits the afferent
discharge of baroreceptors in the aortic arch
and carotid sinus. This stimulates sympathetic
nervous system output. The decrease in blood
volume inhibits the discharge of stretch receptors in the right atrium and also stimulates afferent discharge from chemoreceptors
in the aortic arch and carotid bodies. The resulting increased sympathetic tone causes the
release of catecholamines, epinephrine, and
norepinephrine, intensifying venous tone, increasing heart rate, myocardial contractility,
and subsequently, cardiac output. This compensatory mechanism is an effort to improve
perfusion to the vital organs and tissues,^
It is important to understand, however,
that not all patients in hypovolemic shock
demonstrate tachycardia. Patients who are on
/3-blockers are unable to mount a compensatory tachycardia. Patients who have a concomitant spinal cord injury cannot increase
heart rate in response to volume loss and
hypotension due to inhibition of the sympathetic nervous system,"
This catecholamine release, causing arteriolar constriction, does not affect all systems to
the same degree. The body preserves blood
flow to the heart and brain at the expense
of the gastrointestinal (GI) tract, the skin,
and skeletal muscle. However, if the shock
state persists or worsens, myocardial function eventually becomes impaired. The greatest decrease in circulation during vasoconstriction occurs in the visceral and splanchnic
circulation. Intestinal perfusion is depressed
out of proportion to reduction in cardiac
output,'°
Blood flow to the kidneys is preserved
with a small to moderate hemorrhage; however, the renal vessels will constrict w^ith
large blood loss. Eventually there is a decline in glomerular filtration and urine output. The kidneys require high blood flow
to maintain cellular metabolism. Sustained
hypotension may result in tubular necrosis. Blood flow to the liver is reduced but
to a lesser extent than in peripheral tissue. Decreased circulation to the skin is responsible for the coolness associated with
hypovolemia,^
PLASMA VOLUME
Vasoconstriction causes a shift of fluid
between the vascular compartment and the
interstitial spaces. Normally, there is little
fluid movement between these 2 compartments. In early or compensated shock, there
is a reduction in capillary hydrostatic pressure, w^hich allows movement of protein-free
fluid from the interstitium to the vascular
space, increasing intravascular volume and
decreasing interstitial volume. This extracellular fluid mobilization usually occurs over
a 6- to 12-hour period. It is not responsible
for large volume changes in early phases of
hemorrhagic shock, ^
CRITICAL CARE NURSING QUARTERLY/JANUARY-MARCH
Decreased renal blood flow activates the
renin-angiotensin system, stimulating production of angiotensin I, Angiotensin I is subsequently converted to angiotensin II, a
strong vasoconstrictor that promotes aldosterone release from the adrenal cortex. Simultaneously, angiotensin II potentiates the
action of adrenocorticotrophic hormone on
the adrenal cortex and further promotes
epinephrine release from the adrenal medulla,
Adrenocorticotrophic hormone is released
from the adrenal cortex, increasing renal
sodium and water retention, as well as potassium excretion, which support the intravascular volume. Simultaneously, the posterior
pituitary releases additional antidiuretic hormone, or vasopressin, which promotes reabsorption of solute-free water in the distal
tubules and collecting system of the kidneys. It also further stimulates peripheral
vasoconstriction, ^
CATABOLISM
During shock states, catecholamine output and glucocorticoid production create
a catabolic state. Plasma concentrations of
glucagon rise. Together, catecholamines and
glucagon promote glycogenolysis and lipolysis. As a result, hyperglycemia, as well as elevated lactate and fatty acid levels, may be observed as the shock state progresses.^
ACID-BASE DISTURBANCES
Acid-base disturbances are reflective of
the shock state. Measures of anaerobic
metabolism include serum bicarbonate, pH,
base excess, and lactate. In compensated,
or mild to moderate, shock, the most frequently observed acid-base abnormality is
respiratory alkalosis. It is important to monitor blood gases on a regular basis. Hypoxic
or hypotensive stimulation of the aortic and
carotid chemoreceptors, the presence of
metabolic acidosis, and painful stimuli activate the respiratory center, causing hyperventilation. As the shock state progresses, anaer-
2005
obic metabolism predominates, stimulating
lactate production and subsequent metabolic
acidosis. The resultant metabolic acidosis further exacerbates the shock state, decreasing
sensitivity to catecholamines and stress hormones, resulting in decreased myocardial contractility, promoting predisposition to cardiac
dysrhythmias,^
Lactic acidosis, the physiologic deficit resulting from inadequate perfusion, is reflected
in high serum lactate levels. The amount of
lactate produced correlates with total oxygen
debt, signifying the magnitude of hypoperfusion, the severity of shock, and also adequacy
of resuscitation. Serum lactate is considered
a sensitive indicator of occult shock and may
be useful in patients •with a significant mechanism of injury yet demonstrating vital signs
within normal limits. Since the 1960s, several studies have pointed to increased death
rates associated with metabolic acidosis, as reflected in arterial pH, lactate, and base deficit
clearance,^'^ Base deficit is defined as the
amount of base, measured in millimoles, required to titrate 1 L of whole arterial blood to
a pH value of 7,40, the sample is completely
saturated •with oxygen at 37°C, and has a PCO2
of 40 mm Hg,' Base deficit is used as an index
of the severity of shock in the adequacy of resuscitation, measuring global tissue acidosis.
Some studies suggest a correlation between
base deficit and survival probability, although
others refute this,'^'''
Arterial blood gases assess acid base, ventilation, and oxygenation status in the injured patient. Hypoxemia contributes to tissue oxygen deficit present in hemorrhagic
shock; therefore, measurement of arterial
PCO2 helps drive decision making regarding the need for intubation and ventilatory
support.
Treatments for metabolic acidosis are aimed
at correcting the underlying cause: hypoperfusion. Supporting adequate oxygen delivery
through volume loading, transfusions, and judicious inotropic support are used to achieve
resuscitation goals of normal values in arterial pH, base deficit, lactate, and gastric
Hypovolemic Shock
MONITORING DURING SHOCK AND
RESUSCITATION
Frequent assessment and reassessment
through continuous monitoring is necessary
to identify and correct the causes for circulatory compromise. Cardiac monitoring
should be initiated upon arrival and continued throughout the critical care phase to
monitor and evaluate abnormalities in rate
and rhythm. Persistent tachycardia, despite
aggressive resuscitation efforts, may indicate
ongoing hemorrhage. Rhythm disturbances
may reflect a progressive shock state. Ongoing blood pressure monitoring, pulse
oximetry, core body temperature, and urine
output are all useful in assessing circulatory
status. Urine output reflects renal perfusion
and indirectly, overall central perfusion, A
urine output of 1 to 2 mL/kg per hour is
normal; output of less than 1 mL/kg per hour
suggests inadequate resuscitation and poor
perfusion,^
Central venous pressure monitoring is typically not initiated during early resuscitation,
but may prove useful in patients with prolonged and extensive resuscitation, including massive transfusion. It may be necessary
to establish central venous access in patients
where adequate peripheral intravenous (TV)
access has not been successful. It is also
an adjunctive tool to aid in the diagnosis
of undefined shock or measurement of volume status in patients with CHF or renal
disease.^ Pulmonary artery catheter (PAC)
placement may be considered in the critical
care unit for patients suffering from undifferentiated shock, and to guide volume replacement for patients with comorbid factors
such as congestive heart failure and renal
insufficiency. Consideration for a PAC may
be useful in guiding resuscitation for patients who are not hypotensive, but exhibit
more subtle signs of shock such as cool extremities and elevated lactate levels.''* However, PACs are invasive, time-consuming to insert and maintain, and carry certain risks of
morbidity.
1
OBSTRUCTIVE SHOCK
Obstructive shock refers to a symptom complex where mechanical obstruction interferes
with the ability of the heart to generate adequate cardiac output. Intravascular volume is
sufficient and the heart pumping action is adequate. Basically, "blood can't flow where it
needs to go." The most frequently described
causes of obstructive shock are tension pneumothorax, pericardial tamponade, and pulmonary embolus. Recall our case study. Upon
arrival to the trauma center, the patient was
intubated. However, the respiratory therapist
reported difficulty ventilating the patient, despite the fact that correct endotracheal tube
placement was confirmed. The trauma surgeon performed a needle thoracostomy to relieve intrathoracic cavity pressure for a suspected tension pneumothorax.
In tension pneumothorax, air accumulates
in the intrathoracic cavity, causing compression of the vena cava. As a result, venous return to the heart is compromised, limiting cardiac output. This is a life-threatening situation
and must be corrected immediately,^
In pericardial tamponade, fluid accumulates in the pericardial space, elevating Lntrapericardial pressure and impairing ventricular filling. As a result, stroke volume and
cardiac output are reduced. As aortic pressure falls, coronary blood flow is reduced during a period of increased myocardial oxygen
demand and, as a result, myocardial faUure,
shock, and cardiac arrest may follow.'^
CARDIOGENIC SHOCK
Cardiogenic shock is defined as the inability
of the heart to maintain adequate tissue perfusion secondary to impaired pump function or
failure. In the presence of trauma, cardiogenic
shock is likely the result of an acute myocardial infarction either from pretraumatic event
or from direct myocardial injury, Cardiogenic
shock could also result from transection of a
coronary vessel or chamber injury after a penetrating
^^
8
CRITICAL CARE NURSING QUARTERLY/FANUARY-MARCH 2005
DISTRIBUTIVE SHOCK
Distributive shock describes abnormalities
in vascular resistance, causing maldistribution
of blood flow. Some of the more common
causes are sepsis, anaphylaxis, and spinal cord
injury.
From a pathophysiologic standpoint, low
vascular resistance increases intravascular capacity. This expanded vascular capacity, in the
presence of a normal or low intravascular volume, causes a functional hypovolemia, resulting in inadequate tissue perfusion. Distributive shock is also sometimes termed "warm
shock." Spinal cord injury above the level
of Tl results in almost unopposed parasympathetic tone. These patients do not vasoconstrict and may not demonstrate the cool
clammy skin commonly associated w^ith hemorrhagic shock, Transection of the cervical
spinal cord may impair cardiovascular control. Unopposed vagal tone contributes to the
bradycardia, loss of arterial tone, and the hypotension witnessed in neurogenic shock.^**
Septic shock, resulting from infection, is
unusual in the early stages of acute trauma,
except in the patient presented w^ith grossly
contaminated wounds,'' Septic shock will be
discussed with multisystem organ failure, as it
is a frequent sequela of hypovolemic shock,
DIFFERENTIAL DIAGNOSIS
Shock due to hypovolemia may be confused
with, or confounded by, shock from other
causes. In some instances, there may be more
than one type of shock in play. Consider the elderly patient who may have had a myocardial
event before his car crash, Cardiogenic shock
produces signs and symptoms as those found
in hypovolemia with the exception that the
neck veins are usually distended. However, remember that vein distention may not occur if
there is inadequate circulating fluid volume,
Hypotensive patients who sustain high
spinal cord injuries may be challenging
diagnostically. These patients will exhibit
hypotension secondary to peripheral vasodilation. This type of shock may be relatively re-
sistant to fluid administration. However, the
patient is typically bradycardic because of increased parasympathetic tone and the inhibition of the sympathetic nervous system. The
team must consider the possibility of spinal
cord injury once hypovolemic shock is excluded, How^ever consider the major trauma
patients with multisystem injuries w^ho may
be suffering from both hypovolemic shock
and spinal cord injury. However, it is imperative to assume that shock in spinal cord injury patients is due to hypovolemia, and not
due to neurogenic shock. Only after blood
loss is summarily ruled out, the physician
should consider the diagnosis of neurogenic
Diagnosis is most challenging when more
than one cause is present. Another example
is the patient who suffers a myocardial contusion from blunt trauma and w^ho also has hypovolemic shock from other injuries. Remember that many trauma patients suffer injuries
to more than one system.
Drug and alcohol intoxication may also
make the diagnosis of hypovolemia troublesome. Serum ethanol elevation causes the skin
to be warm, flushed, and dry. Urine is usually dilute. These patients may be hypotensive when supine, with exaggerated changes
in postural blood pressures measurements,
Hypovolemic shock victims present as cold,
clammy, oliguric, and tachyeardic,^''
Treatment priorities
Throughout every phase of trauma care,
the priorities of airway, breathing, and circulation are paramount. Problems encountered
in these areas must be addressed rapidly and
sequentially. Sources of bleeding are continually assessed, Hemodynamic monitoring is
performed on a continuous basis and changes
reported to the trauma-attending physician.'"
FLUID RESUSCITATION
In the ICU, fluid resuscitation is carried
out in a more controlled fashion than in the
acute posttraumatic situation. During initial
Hypovolemic Shock
resuscitation attempts, IV access is obtained
through the use of at least 2 large bore (14-16)
gauge or larger catheters. Femoral cordis lines
are commonly used in our institution when
there are no contraindications for using this
site. The small ports on the pulmonary artery
and triple-lumen catheters are typically inadequate for rapid fluid resuscitation and should
be used only after other large bore catheters
are in place,
INITIAL FLUID MANAGEMENT
The goal of fluid administration in the
trauma patient is to replace volume in order to support cardiovascular function by increasing cardiac preload and to maintain adequate peripheral oxygen delivery,'' Rapid fluid
resuscitation is considered the cornerstone
of therapy by some for the initial management of hypovolemic shock,^ However, there
has been controversy over the years regarding the aggressive administration of TV fluids to hypotensive patients with penetrating
torso wounds. Research studies from the early
1990s suggest that IV fluids should be delayed until the time of definitive operative
intervention, '^' "^
In young patients, volume infusion is typically infused at the maximum rate allowed by
the equipment and the size of the cannulated
vein until a response is appreciated. In older
patients or those with comorbid conditions
such as cardiac disease, fluid resuscitation is
titrated to response to avoid complications associated with hypervolemia,'°
Attempting to reach normotension by the
transfusion of resuscitation fluids is not necessarily the goal. Much time can be lost chasing vital signs with fluid resuscitation when,
in some injuries, early definitive operative intervention to stop blood loss is required,
CYSTALLOIDS VERSUS COLLOIDS
Parenteral solutions for the IV resuscitation
of hypovolemic shock are classified as crystalloid or colloid, depending on molecular
weight. Controversy exists regarding the appropriate choice of resuscitation fluid for the
trauma victim with mild to moderate hemorrhage. The focus of this controversy centers primarily on the effect each fluid type
has on the lungs. Proponents of colloid therapy argue that maintenance ofthe plasma colloid oncotic pressure (PCOP) is necessary to
minimize interstitial edema, particularly Ln the
lungs. The concern is that massive crystalloid
resuscitation creates an oncotic pressure gradient encouraging movement of fluid from
the intravascular space into the pulmonary
interstitium. Colloid supporters further propose that since colloids remain primarily in
the intravascular space, they are more effective volume expanders, and also are less likely
to cause peripheral edema than crystalloids.
However, little support is found in the literature to support superior efficacy of one solution over the other.^'^
CRYSTALLOIDS
Crystalloid solutions are generally safe and
effective for resuscitation of patients in hypovolemic shock. Isotonie human plasma solutions, with sodium as the principal osmotic
active particle, are used for resuscitation.
They can be administered rapidly through peripheral veins due to their low viscosity. Isotonie fluids have the same osmolality as body
fluids; therefore, there are no osmotic forces
directing fluids into, or out of, intracellular
compartments. During resuscitation, isotonie
crystalloids are administered approximately
3 to 4 times the assessed vascular deficit to
account for the distribution between the intravascular and extravascular spaces. Crystalloids partition themselves in a manner similar to the body's extracellular w^ater content;
75% extravascular and 25% intravascular The
majority of complications associated with
the use of crystalloid solutions are either
because of undertreatment or because of
overtreatment.'^'"'' '^
The use of one specific crystalloid over another is largely a matter of institutional or
10
CRITICAL CARE NURSING QUARTERLY/JANUARY-MARCH
provider preference. Normal saline is the only
crystalloid that can be mixed with blood and
blood products. Patients resuscitated with
large amounts of normal saline are at risk
for developing hyperchloremic metabolic acidosis because its chloride concentration is
higher than that of plasma. Lactated Ringer's
solution has the advantage of a more physiologic electrolyte composition.
Hypertonic saline solutions are crystalloids
that contain sodium in amounts higher than
physiologic concentrations. They expand the
extracellular space, by creating an osmotic
effect that displaces water from the intracellular compartments. Hypertonic saline decreases wound and peripheral edema. There
is some research to suggest, however, that hypertonic saline resuscitation may contribute
to increased bleeding.^''*'"'
Most sources agree that the best way to
manage hypovolemic shock in trauma patients is the judicious use of w^armed TV fluids
and blood products. Many trauma centers initially infuse 2 to 3 L of lactated ringers or normal saline and then consider blood products if
the patient remains symptomatic. While crystalloids are infusing, the blood bank has time
to type and cross-match the patient for transfusion of type-specific blood.'°"
COLLOIDS
Colloids are solutions that have a highermolecular-weight species and create an osmotic effect. Colloids remain in the intravascular space for longer periods than
do crystalloids. Smaller quantities are required to restore circulating blood volume.
Colloids attract fluid from the extravascular to the intravascular space because of
their oncotic pressure. Examples are albumin,
hetastarch, dextrans, modified fluid gelatin,
and urea bridge gelatin. They are expensive to use and complications have been reported Ln their use. Albumin has been implicated in decreased pulmonary function,
depressed myocardial function, decreased
serum calcium concentration, and coagulation abnormalities.'" Hetastarch may cause
2005
decreased platelet count and prolongation of
the partial thromboplastin time. Several complications have been associated with the use
of dextran, to include renal failure, anaphylaxis, and bleeding. Gelatins are associated
with anaphylactoid reactions. They also may
cause depression of serum fibronectin. Because ofthe high cost and complication rates,
there appears to be no clear advantage to using colloid solutions,'*'"'
Blood products and component therapy
Neither crystalloid or colloid solutions increase oxygen-carrying capacity. Administration of large amounts of fluids can also prove
detrimental by diluting hemoglobin levels and
contributing to fluid volume overload.''
Blood products are currently the most readily available fluids to increase oxygen-carrying
capacity and cardiac preload. However, transfusions carry the risk of various blood-borne
pathogens and transfusion reactions. There
is considerable debate regarding indications
for transfusion. Patients with hemorrhage of
up to approximately 20% of their total blood
volume can be safely volume replaced with
crystalloids in a ratio of 3 mL of crystalloid
per milliliter of estimated blood loss. During the infusion of crystalloids, the blood
bank has time to perform a type and crossmatch, so that, if needed, type-specific blood
is available for transfusion. Most agree that
patients with 20% to 40% loss of circulating
blood volume, or those demonstrating evidence of hemodynamic instability, and those
with blood gas evidence of shock, despite aggressive fluid resuscitation, may benefit from
blood transfusions,^'^
BLOOD TYPES AND Rh ISSUES
The decision to transfuse should be based
on the assessment of ongoing blood loss, the
patient's ability to compensate, and the availability of cross-matched blood products. Additional considerations are given to the patient's age and presence of comorbidities,^
Ultimately, type-specific blood products are
Hypovolemic Shock
preferred, but w^hen a patient arrives in apparent shock or extremis, the universal donor
type O, Rh negative, is transfused using a rapid
infusor/warmer device.
Rh-negative blood may be in short supply; therefore, some hospitals have policies in place that allow Rh-positive Group
O, packed red blood cells (PRBCs) to be
transfused in men, and women older than
childbearing age. The rationale behind this
practice is that naturally occurring anti-Rh
bodies do not exist, therefore there is no advantage to the use of Rh-negative blood. However, there is some concern that Rh-negative
patients may have been sensitized from pregnancy or previous transfusions and could develop a delayed hemolytic transfusion reaction from Rh-positive blood use. This is a rare
occurrence; therefore, O-Rh-positive PRBCs
are considered the first choice for emergency
transfusions, with consideration for the use of
O-Rh-negative PRBCs for females with childbearing potential.^ Some sources recommend
that the number of transfusions of type O be
limited to 4 units, after which type-specific
blood should be available in most institutions
receiving trauma patients. However, when
necessary, type O blood may be continued
until the patient stabilizes or type specific is
Type-specific blood is ABO and Rh compatible and is available within less than 15 minutes in most institutions. Type-specific blood
has been shown to be safe and effective during emergency resuscitations. 18
MASSIVE TRANSEUSION
Trauma practitioners are frequently faced
with situations that require decision making
to weigh the risks and benefits of massive
transfusions. When the decision is made to
proceed, there are technological considerations that affect infusion rates. Large bore
catheters, as well as high-volume IV tubing, allow for the fastest blood administration. Pressure bags and/or mechanical rapid transfusion
devices further increase flow rates. Remember that normal saline is the only fluid additive
11
that can be used in conjunction with blood
product transfusion, Lactated Ringer's solution w^ill cause precipitation of blood w^ithin
BLOOD COMPONENT THERAPIES
At this writing, component therapy remains
the current standard for blood transfusion.
It refers to the utilization of the components of whole blood to include RBCs, fresh
frozen plasma (FFP), platelets, and cryoprecipitate. One unit of whole blood contains
200 mL of red blood cells and 250 mL of
plasma, which contains coagulation factors.
Component therapy has several advantages
over whole blood, and evidence suggests that
the PRBCs and component therapy are as
effective as whole-blood transfusion without
the disadvantages. PRBCs and components
are more readily available and are less expensive and easier to store than whole blood. Volume expansion can be accomplished w^ith a
combination of crystalloids and PRBCs, Another advantage of component therapy over
whole blood is that infusions can be tailored
specifically to the needs of the individual patient. Furthermore, PRBCs increase oxygencarrying capacity more efficiently than whole
blood. The disadvantage of whole blood is
that platelets are not w^ell preserved, and clotting factors decrease rapidly at blood storage
temperatures. For these reasons, PRBC infusion with component therapies are considered the methods of choice for increasing red
blood cell mass and oxygen-carrying capacity
in hemorrhagic shock,^
COMPUCATIONS OF TRANSFUSIONS
Blood-borne pathogens
Improved screening has significantly
decreased the incidence of blood-borne
pathogens or transfusion-transmitted diseases
(TTDs),-^ However, they still contribute to
the incidence of late death from transfusion.
Increased awareness and concerns related
to TTDs, especially HIV infection, have
12
CRITICAL CARE NURSING QUARTERLY/JANUARY-MARCH
prompted caution and reconsideration of
blood transfusion indications. Hepatitis B is
the most common infectious complication.
Before testing for hepatitis C, non-A non-B
hepatitis was the most frequent infectious
complication,'^
Transfusion reactions
Transfusion reactions are categorized into
hemolytic and nonhemolytic types. Major
hemolytic transfusion reactions occur as a result of the interaction of antibodies in the
plasma of the recipient with antigens present
in the red cells of the donor. It is important
to stress that the majority of hemolytic reactions are due to clerical error in the identification of blood samples or in the administration of properly cross-matched blood to the
wrong patient. During high-stress situations
of massive transfusion administration, meticulous attention must be paid to the processes
surrounding blood banking and blood product administration to avoid this preventable
complication,'^
Nonhemolytic transfusion reactions are
more common and related to reactions to
leukocytes or proteins in the donor blood.
These may be mitigated by premedication
with antipyretics and antihistamines. Typical reactions may be mild, consisting of rash
or nuld bronchoconstriction. More rare are
severe responses such as subglottic edema,
severe bronchoconstriction, and anaphylaxis
with cardiovascular collapse,'^
Platelet and coagulation factors
Along with the previously mentioned concerns for blood-borne pathogens and transfusion reactions, there are several other
complications related to blood product transfusions, with higher complications rates associated with massive transfusion therapy, often
considered 10 U or more. Massive transfusion
of blood products and concurrent infusion of
large volumes of crystalloid cause certain
hematologic and physiologic consequences.
Not only do coagulation factors and platelet
numbers and function diminish during RBC
2005
storage, the massive blood and fluid administration further dilutes the number of circulating platelets. This dilutional thrombocytopenia causes clotting abnormalities. It is
important to assure that there is appropriate and timely administration of platelets and
FFP to prevent this complication. Treatment
should be based on clinical evidence of impaired hemostasis, by following prothrombin
time, partial thromboplastin time, and platelet
count. While circulating platelet counts of
20,000 per mm^ or fewer may be adequate
in nonbleeding patients, platelet transfusion
is appropriate for patients with evidence of
ongoing microvascular bleeding with levels of
100,000 per mm' (see references 4 and 19),
Massive transfusion therapy can contribute
to significant electrolyte and acid-base disturbances. Among these are hypocalcemia, hyperkalemia, and hypokalemia, Hypocalcemia
occurs during massive transfusion, because
each unit of PRBCs contains citrate, which
binds to ionized calcium in the blood. Large
citrate doses may be toxic and can precipitate hypocalcemia. Clinical signs of hypocalcemia include prolongation of the QT segments on ECG, skeletal muscle tremors, and
perioral tingling. Calcium levels should be
closely monitored during massive transfusion therapy. Citrate also may contribute
to hypomagnesemia. Because of this relationship, treatment of hypocalcemia and
hypomagnesemia includes concomitant use
of calcium chloride and magnesium chloride in massive transfusion, based on measured serum levels; empiric treatment is not
Banked blood contains significantly elevated potassium levels because of cell lysis
that occurs during the collection and storage of blood, Hyperkalemia, however, is rare
during massive transfusion, because packed
cells quickly reestablish their ionic pumping mechanism and potassium is rapidly absorbed. In actuality, hypokalemia occurs more
frequently secondary to transient metabolic
alkalosis occurring during massive transfusion, which causes potassium to move into
the
^'^
Hypovolem ic Shock
Acid-base disorders are commonly associated with large volume transfusions. Even
though banked blood is acidic because of its
citrate content, metabolic acidosis is not typically a result ofthe transfusions, but is related
to underlying hypovolemic shock. Treatment
should concentrate on improving tissue perfusion and oxygenation as well as an ongoing
search for underlying sources of hemorrhage.
Sodium bicarbonate administration is not recommended and has several detrimental side
effects. In rare circumstances, a trauma patient may have metabolic acidosis due to a
cause other than hypovolemia, such as comorbid factors to include diabetic ketoacidosis,
carbon monoxide (CO) poisoning, drug, or
toxic ingestion,^
13
HYPOTHERMIA
fusions, and exposure of body cavities during
surgery.'
Gentilello classifies hypothermia in trauma
patients into 3 risk categories based on core
body temperature. Mild hypothermia (34°C36°C) accelerates oxygen consumption in
an at-risk patient population. Moderate hypothermia (32°C-34°C) further slows physiologic functions. Severe hypothermia (<32°C)
is considered a life-threatening emergency.^'
There are a number of adverse clinical effects related to hypothermia. These are cardiac dysrhythmias, reduction in cardiac output, increasing systemic vascular resistance,
increased lactic acid production, and coagulopathic bleeding. Hypothermia has a deleterious effect on the oxyhemoglobin dissociation
curve, shifting it to the left, w^hich impairs
oxygen delivery and worsens the shock
Hypothermia is a serious consequence
of massive blood product transfusion. Progressive core hypothermia with persistent
metaboUc acidosis is the precursor of severe and ongoing coagulopathy states,^ There
are complex pathophysiologic interactions
at play that contribute to impaired coagulation. Mikhail refers to the physiologic limits of the body in response to hypovolemic
shock as "the trauma triad of death"; hypothermia, acidosis, and coagulopathy' Hypothermia has been strongly implicated in
the development of acidosis and is frequently
demonstrated as a consequence of severe injury and routinely prescribed resuscitation
efforts,'"^ Studies suggest that as many as two
thirds of all trauma patients arrive at emergency departments with hypothermia, regardless of geographic locale,'^*' Many trauma patients develop hypothermia at some point
in their treatment and this is poorly tolerated. Hypothermia occurs in trauma patients
with minimal cold stress secondary to inadequate tissue oxygenation and perfusion,
preventing the body from generating enough
heat to maintain normothermia,^' Predisposing factors are age, injury severity, impaired
thermogenesis, elevated serum alcohol levels, fluid resuscitation, blood product trans-
Many research studies have directly linked
the presence of hypothermia in trauma patients with high mortality rates.'^"^' The primary goal is to identify those patients at risk
and to intervene in this cycle of hypothermia,
acidosis, and coagulopathy' Core temperature should be monitored continuously. At our
institution we use a foley catheter with a thermal measuring device that provides continuous core temperature measurement. Efforts
to prevent hypothermia should be employed
such as using a high-volume fluid warmer during massive transfusion therapy.
Based on these findings, the surgical approach to the care of the severely injured
trauma patient has changed over time. Early
on, the goal of trauma surgeons was to provide definitive operative intervention by performing a traditional exploratory laparotomy,
where all injuries were identified and repaired. Patients would spend long periods
of time in the operating room, receiving fluids, blood products, and with open peritoneum, resulting in core thermal temperature loss. Predictable evaporative heat loss
with an open peritoneum, despite state-ofthe-art resuscitation procedures, is 4,6°C per
hour,^^ Patients w^ould leave the operating
room cold and coagulopathic. Currently the
14
CRITICAL CARE NURSING QUARTERLY/JANLIARY-MARCH
goal in trauma operative resuscitation is to
perform "damage control" or staged laparotomy. This initial procedure is abbreviated
and intended to control hemorrhage and contamination, pack the abdomen, perform temporary closure of the abdominal wall, and
move the patient quickly to the ICU for further stabilization and rewarming procedures.
Stopping or abbreviating the initial procedure
allows the trauma team to correct coagulopathy, maximize oxygen delivery, and reverse acidosis and hypothermia. Following
stabilization in the ICU, the patient can return to the operating room for a more controlled completion ofthe surgical procedure,^
Again, the goal is to prevent the triad of hypothermia, acidosis, and coagulopathy, because of the high mortality associated with
this syndrome,' As we compress the time
frames through which we move our patients
tow^ard definitive operative intervention, it
is imperative that critical care nurses understand their role in intervening in this
pathogenesis.
Rewarming techniques
The selection of rewarming techniques is
based on how severely hypothermia is affecting the patient. Stable patients who are mildly
hypothermic, and without life-threatening injuries, are typically treated with passive external rewarming techniques. Passive rewarming
techniques involve removing wet clothing, increasing ambient room temperature, decreasing airflow^ and insulating the patient, and allowing his or her metabolic heat to increase
body temperature.
Active external rewarming techniques include warm fluid circulating, convection air,
"space blankets," and radiant heat lamps.
Head covering is important, as 50% of radiant heat loss occurs from the scalp. These
strategies are typically more effective in preventing hypothermia than in treating it. It
should not be the sole source of rewarming
for patients exhibiting an adverse response to
hypothermia, as results are not immediately
effective.
2005
Active core rewarming techniques include
the administration of warmed humidified air,
heated body cavity lavage to include peritoneum and pleura, and warmed IV fluid
infusion and blood transfusions. Patients requiring large boluses of fluid for resuscitation as well as blood products can receive a
substantial amount of heat through warm IV
fluids,
Extracorporeal circulatory rewarming techniques, such as cardiopulmonary bypass,
venovenous, or arteriovenous, are the most efficient rew^arming methods. However, they require large bore vessel cannulation, especially
trained technician and dedication to the duty.
Therefore, these procedures are typically restricted to a few tertiary centers.^'
Coagulopathy
Coagulopathy, or hypocoagulability after
major trauma, is common in severely injured
patients and recognized as a major cause
of early death. There are many contributing factors, and the pathophysiologic relationships are complex. Little progress has
been made in correcting this phenomenon
once it develops. Virtually all normal physiologic clotting mechanisms are severely deranged in the cold, acidotic, bleeding trauma
patient. The clotting cascade, governed by
a series of temperature sensitive reactions,
is inhibited during episodes of hypothermia.
Clotting abnormalities are exacerbated when
core body temperature falls below 34°C,
Platelet function is also affected by lo^w body
temperatures.
Treatment for hypovolemia includes infusion of cystalloids and blood products, Coagulopathy becomes clinically important during
massive transfusion therapy. Coagulation factors are rapidly depleted. During shock, hepatic function is impaired, impacting the ability
ofthe liver to rapidly mobilize additional coagulation factors. Prothrombin time and partial
thromboplastin time should be carefully monitored. Transfusion of FFP and platelets should
be administered on the basis of the results of
coagulation profiles."*
Hypovolemic Shock
BLOOD SUBSTITUTES
Despite advances in detecting TTDs, concerns StiU remain regarding the risk of
transmitting hepatitis and human immunodeficiency virus (HIV) during transfusion
therapy. There are reports of PRBC count
shortages every year, and storage of red blood
cells has finite limitations. As a result, there
is a great deal of interest in the development
of blood substitutes as an alternative choice
in the treatment of hypovolemic shock. Unlike blood, hemoglobin substitutes require
no cross-match, have a long shelf life, and
reportedly carry no risk of blood-borne viral pathogens. Additionally, since they have
a lower viscosity than blood, flow through
small capillaries may be enhanced, which potentiates peripheral oxygen delivery,'*''^' Preclinical studies showed hemoglobin substitutes to be as effective as blood and more
effective than standard colloid or crystalloid
solutions for resuscitation from hemorrhagic
and septic shock. The hope was to provide
an immediate on-site replacement for traumatic blood loss, prevent tissue ischemia and
organ failure, and provide effective hemodynamic support for septic-shock-induced
hypotension.^'••^'*
Recent research supports the concept that
postinjury multiple organ failure is related
to inflammatory response. Biologic mediators present in stored blood have been implicated in early postinjury hyperinflammatory syndrome and multiple organ failure
through priming of circulating neutrophils.
Some newer hemoglobin-based substitutes
are free of priming agents and may provide an alternative to transfusing PRBCs in
the early postinjury phase,^^•^'*'^^ Humanpolymerized hemoglobin (PoIyHeme®) is a
universally compatible, pathogen-free, readily available, oxygen-carrying blood substitute
being developed for use in case of urgent
blood loss. Recent study shows that this compound increases survival in patients with lifethreatening red blood cell levels by maintaining hemoglobin levels in the absence of red
cell transfusion,'^' The Food and Drug Admin-
15
istration has approved transfusion of up to
10 consecutive units of polytteme for acute
bleeding. Stage 3 clinical trials are currently
in process in several trauma centers,
SHOCK SEQUELAE
Systemic inflammatory response
syndrome
Systemic inflammatory response syndrome
(SIRS) describes the pathophysiologic response to a cascade of events precipitated
by shock. Usually after trauma, a controlled
inflammatory response occurs, which is designed to heal wounds and w^ard off infection.
However, continuous stimulation or severe infection may result in a sustained inflammation
(SIRS), The result is an imbalance of cellular
oxygen supply and demand, which results in
oxygen extraction deficit. This inflammatory
response may occur without any source of
bacterial infection.^
Overwhelming SIRS occurs with persistent
stimulation disrupting anaerobic cellular cycles. Disruption in the process of cellular
metabolism promotes a cascade of events including promotion of adhesion of molecules,
catecholamines, chemotaxis, and a coagulation cascade. There is an accompanying decrease in vascular resistance resulting in profound increased cardiac index, designed to
promote oxygen delivery and cellular oxygen uptake. This hypermetabolic demand,
coupled with acute deficit in oxygen extraction and metabolic failure, is precursors of multiple organ dysfunction syndrome
MODS
Historically, infection has been considered
the cause of SIRS and MODS. Typical sources
of infection are IV catheters placed in the prehospital environment or emergency department. Also implicated are urethral catheters
and endotracheal tubes. Decreased gastric
acid allows for increased numbers of bacteria to survive and multiply, theoretically,
allowing translocation of bacteria in the
16
CRITICAL CARE NURSING QUARTERLY^ANUARY-MARCH
distal bowel, theoretically resulting in high
pneumonia rates,^^
Studies show that approximately 60% of
trauma patients will have clinical signs of
sepsis without an apparent bacterial source.
Sepsis, and the ensuing multiple organ failure, remains a leading cause of death in
the surgical ICU, despite significant advances
made regarding the management of trauma
victims.^^ Sepsis is characterized by increased
oxygen consumption, and increased cardiac index w^ith decreased vascular resistance. These are indicators of the hyperdynamic cardiovascular state associated with
sepsis,'
The process of an uncontrolled inflammatory response with a progression to MODS
is recognized as a defect in cellular signaling. Recall the previous discussion of trimodal
death patterns following major traumatic injury. Late deaths may occur 5 to 4 weeks after the initial shock episode. Inadequate early
resuscitation has been implicated in the cascade of acidosis, hypothermia, and coagulopathy. This triad leads to multisystem organ failure and death. Lee and others describe
the initial response to shock and development of SIRS, followed by progressive organ
failure. This continuum is initiated and perpetuated by inflammation and inflammatory
mediators.^^
These topics are complex, requiring indepth discussion and, as such, are beyond the
scope of this overview article, How^ever, it is
important for the critical care nurse to explore ongoing research regarding cytokines,
complement activation, and lipid mediators.
Studies are currently adding to the body of
knowledge regarding inflammatory response
and multisystem organ failure after hypovolemic shock.
As compensatory mechanisms continue to
fail, tissue ischemia results from hypoperfusion as blood flow is shunted away from tissues with high metabolic demands, either
from microvascular injury or from inflammatory response. Organ system failures commonly seen are pulmonary, hepatic, and renal
failure. When 3 or more systems are affected.
2005
the mortality rate climbs as high as 80% to
End points of resuscitation
At what point does one determine that resuscitation is complete? Many researchers use
the same clinical, physiologic, or laboratory
studies to identify subtle hypoperfusion and
to determine when adequate or normal perfusion resumes following resuscitation. Typical
end points are blood pressure, heart rate, and
urine output,'"^ However, recent studies suggest tissue hypoperfusion can persist despite
normal vital signs. Cardiac and pulmonary
function can be monitored fairly accurately in
the ICU with current technology. By contrast,
tissue perfusion, which represents circulatory
function ofthe peripheral tissues, is measured
indirectly by a variety of subjective symptoms,
such as vital signs, pulse rate and quality, skin
temperature, color, and moistness as well as
mental status. These assessments are routinely
used to infer circulatory status and tissue perfusion, but they are not direct quantitative
measurements of tissue perfusion, ^^ The challenge is to identify those patients at risk for
hypoperfusion; it may be present despite normal cardiac indices,^'* Other modes of assessment, to include gastric tonometry, transcutaneous oxygen, and CO2 measurements, are
currently being utilized as early warning signs
of tissue hypoxia and hemodynamic shock in
critically ill patients.'"
If we go back and review the defmition
of shock as the consequence of insufficient
tissue perfusion, resulting in inadequate cellular oxygenation, what parameters do w^e
choose to measure cellular oxygenation and
tissue perfusion? In patients with inadequate
tissue perfusion, oxygen delivery is insufficient for the generation of adenosine triphosphate. Without adenosine triphosphate, the
body cannot sustain normal cellular function. Anaerobic metabolism and tissue acidosis are results, CO2 levels increase in the
splanchnic or gut circulation. Successful resuscitation from shock is measured by a limitation of oxygen debt and tissue acidosis
Hypovolemic Shock
with the return of aerobic
Clinicians rely upon both global and organspecific parameters to measure end products
of inotropic metabolism to determine if complete resuscitation has been achieved. Basically, global indexes measure overall degree of
hypoperfusion, based on a number of readily
available data sets. Some of these include the
following.
Oxygen delivery index
Oxygen delivery index (DO2D (normal
value 500-600 mL/min/m^) is determined by
CO (carbon monoxide), hemoglobin saturation, and the ability of the lungs to load oxygen onto the hemoglobin molecule. In severe
hemorrhagic shock, there is a decrease in circulating hemoglobin, which influences this
component of oxygen delivery.
Cardiac output is affected by several clinical
conditions related to trauma, to include acute
myocardial infarction, hypovolemia, septic
shock, neurogenic shock, cardiac contusion,
and pericardial tamponade.
Pulmonary function relative to oxygen
delivery is affected by the presence of
pneumothorax, hemothorax, flail chest, pulmonary contusion, loss of effective airway, inadequate mechanical ventilation, and other
sequelae of trauma, to include pneumonia,
atelectasis, excessive secretions, and patient
positioning. In a severely injured patient, it
is common to exhibit abnormal DO2I values based on any, or all, of these clinical
factors.
The oxygen consumption index value
(normal value, 125 mL/min/m^) may measure 4 or 5 times the norm in a critically
injured patient. Some causes of increased
VO2I include pain, agitation, posturing,
fever, increased w^ork of breathing, and
tachycardia.
Mixed venous oxygen saturation
Continuous mixed venous oxygen saturation (SVO2) monitoring reflects how much
oxygen was consumed by the tissues. Patients
17
requiring aggressive resuscitation will demonstrate abnormally low values because of either inadequate oxygen delivery or excessive
oxygen demand by the tissues. Normal values for SVO2 are between 65% and 80%; when
values fall below 50%, anaerobic metabolism
is present, A low VO2 tells us that the patient is underresuscitated, or still in shock, but
it is nonspecific as to the cause. This technology requires invasive monitoring via a PA
catheter, which is associated with significant
morbidity to include improper catheter placement, pneumothorax, infection, and equipment malfunction,^^
Arteriovenous carbon dioxide gradient
The gradient between arterial and mixed
venous PACO2 levels reflects the degree and
duration of hypoperfusion and is an excellent barometer of the degree of hypovolemic
shock. Normally, CO2 is cleared Ln the pulmonary circulation, but in profound shock
there is a decrease in cardiac output and poor
pulmonary blood flow, resulting in an accumulation of PACO2 in the tissues, A gap greater
than 11 mm Hg suggests severe compromise.
While arteriovenous carbon dioxide gradient
(AVPACO2) provides a general assessment regarding the effectiveness of resuscitation efforts, it does not provide specific organic
information,^'^
There have been recent technological advances that may provide more information regarding organ-specific or regional
resuscitation effectiveness. These are tonometry, capnometry, and near-infrared spectroscopy. We will discuss their use in measuring specific intracellular tissue response to
resuscitation.
Gastric tonometry
Gastric tonometry assesses gastric mucosal
pH as a marker of the adequacy of resuscitation, evaluating perfusion at the splanchnic bed. The GI tract is very sensitive to
any decrease in circulating volume and may
significantly compromise gut perfusion. This
18
CRITICAL CARE NURSING QUARTERLY/JANUARY-MARCH
technique involves the use of a nasogastric
tube with a saline-filled, gas-permeable silicone balloon at the tip to measure CO2 emitted from the gastric cells, PACO2 is then converted to a pH value. A pH value less than 7,35
suggests anaerobic metabolism, a potentially
negative predictor of adequate splanchnic
perfusion, raising the patient's risk for MODS
and sepsis. Studies however are not conclusive, yet there are indications that gastric
tonometry warrants consideration as a useful assessment tool in measuring gastric tissue
perfusion.^^
Subiinguai capnometry
Recent research involving both animal and
human subjects suggests that measurement of
the proximal GI tract using sublingual PACO2
strongly correlates with decreases in distal gut
blood flow and increases in lactic acid during shock states. Since it is a relatively simple,
noninvasive procedure, it has potential as an
early triage resuscitation tool,'^'^ A microelectrode CO2 probe is placed under the tongue,
providing continuous information regarding
tissue perfusion ofthe proximal GI tract. Continued research is necessary, but early indicators are promising.
Near-infrared
spectroscopy
Near-infrared spectroscopy is another technology on the horizon that may show promise
as a guide to end points of resuscitation.
Minimally invasive, it measures intracellular
oxygen levels, quantifies intracellular function, and identifies other conditions that
may affect intracellular metabolism,^^ It assesses the absorption of infrared light by saturated hemoglobin molecules and cytochromea,a^. It works by passing light waves via
probes through muscle tissue. The device
displays levels of saturated hemoglobin and
cytochrome-a,a3 to alert providers to organspecific hypoxia or to indicate successful
resuscitation efforts through the reappearance of reflected red light. It holds promise
2005
in predicting patients at risk for multisystem organ failure early in the course of
resuscitation.
Both global parameter management such
as SVO2, lactate, and base deficit are helpful
in determining decompensation or improvement in resuscitation states. Care providers
should not be lulled into a false sense
of security, when vital signs and basic
hemodynamic parameters fall within normal limits during resuscitation. New technologies measuring regional tissue perfusion
may be an adjunct tool in this assessment
process. 29
SUMMARY
Shock is a complex physiologic state, resulting in extreme dysfunction of cellular biochemistry, resulting inadequate tissue perfusion, and cellular death, Hypovolemic shock
is most commonly seen in major trauma patients, although the major trauma victim is additionally at risk for cardiogenic, obstructive,
and distributive shock. Differential diagnoses
can be complex.
Resuscitation from shock is restoration
of adequate tissue perfusion. Early identification and aggressive treatment is necessary to prevent or mitigate the effects of
shock states, SIRS and MODS, Current therapies are not without controversy. Ongoing
research is aimed at further understanding the complex biochemical and physiologic responses to shock, to guide further development of appropriate treatment
methodologies.
The critical care nurse remains a key member of the trauma team as resuscitation measures are continued into the critical care environment. It is imperative that the critical
care nurse understand the trauma patient's
complex physiologic response to injury, be
familiar with methods to monitor for key
indicators of shock states, and respond as
a team member to provide timely and aggressive treatment to achieve positive patient
outcomes.
Hypovolemic Shock
19
REFERENCES
1, Mower-Wade D, Bartley M, Chiari-Allwein J.
Shock: do you know how to respond? Nursing.
2000;30(10):34-40,
2, Stern SA, Bobek EM, Resuscitation: management
of shock. In: Ferrera PC, Colucciello SA, Marx JA,
et al,, eds. Trauma Management: An Emergency
Medicine Approach. St Louis: Mosby; 2001:75102,
3, Bell RM, Krontz BE. Initial assessment. In: Mattox KL,
Feliciano DV, Moore EE, eds, Traunia. 4th ed. New
York: McGraw-HiU; 2000,
4, Scalea TM, Boswell SA. Initial management of traumatic shock. In: McQuillen K, Von KA, Rueden KT,
Nartsock RL, Flynn MB, Whalen E, eds. Trauma
Nursing: From Resuscitation Through Rehabilitation. 3rd ed. Philadelphia: WB Saunders; 2002:201221,
5, Mikhail J, The trauma triad of death. AACN Clin Issues. 1999;10(l):85-94.
6, Cairns CB. Rude unhinging of the machinery of life:
metabolic approaches to hemorrhagic shock. Curr
Opin CritCare. 2OOl;7(6):437-443,
7, Muliins RJ. Management of shock. In: Mattox KL,
Feliciano DV, Moore EE, eds. Trauma, 4th ed. New
York: McGraw-Hill; 2000:195-229.
8, Advanced Trauma Ufe Support Course for Doctors {Instructor Course Manual). Shock. 6th ed.
Chicago: American College of Surgeons; 1997.
9, Vary TV, McLean B, Von Reuden KT. Shock and
multiple organ dysfunction syndrome. In: McQuillen
K, Von KA, Rueden KT, Nartsock RL, Flynn MB,
Wlialen E. eds. Trauma Nursing: From Resuscitation Through Rehabilitation. 3rd ed. Philadelphia:
WB Saunders; 2002:173-200.
10. Bongard FS. Shock and resuscitation. In: Bongard
FS, Sue DS, eds. Current Critical Care Diagnosis
and Treatment. 2nd ed. New York: Lange Medical
Books/McGraw-Hill; 242-267; 2002.
11. Cohen S. Shock. In: Cohen S, ed. Trauma Nursing
Secrets. PhUadelphia: Hanley and Belfus; 2003:109114,
12. Davis JW, Shackford SR, Holbrook TL. Base deficit
as a sensitive indicator of compensated shock in
tissue oxygen utilization. Surg Gyencol Obstet.
1991;173:473-476.
13. Husein FA, Martin MJ, MuUinex PS, Steele SR, Elliot
DC. Serum lactate and base deficit as predictors of
mortality and morbidity. Am f Surg 2003;185(5):
484-491,
14. Kaplan LJ, Me Partland K, Santora TA, Trooskin SZ.
Start with a subjective assessment of skin temperature to identify hypoperfusion in intensive care unit
patients./ Trauma. 2001;50(4):620-628.
15. Bickell WH, Wall MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. A' FnglJ Med.
1994;331:1105-1109,
16. Trunkey DD. Prehospital fluid resuscitation. In:
Trunkey DD, Lewis FR Jr, eds. Current Therapy of
Trauma. 4th ed. Chicago: Mosby; 1999:129-130.
17. Schierhout G, Roberts I, Alderson P, Bunn F, Colloids
versus crystalloids for fluid resuscitation in critically
ill patients, Cochran Database SystRev. 1999;3.
18. Moore EE, Mattox KL, Feliciano DV Transfusion,
autotransfusion, and blood substitutes. In: Moore
EE, Mattox KL, Feliciano DV, eds. Trauma Manual.
New York: McGraw-Hill; 2003:84-90,
19. Rotundo MF, Reilly PM. Bleeding and coagulation
complications. In: Mattox KL, Feliciano Dy Moore
EE, eds. Trauma. 4th ed. New York, McGraw-Hill;
2000:1267-1285.
20. Luna GK, Maier Ry Pavlin EG, Anardi D, Copass MK,
Oreskovich MR. Incidence and effect of hypothermia in seriously injured patients, / Trauma. 1987;
27:1014-1018,
21. Gentilello L. Hypothermia in trauma. In: Trunkey DD,
Lewis FR, eds. Current Therapy of Trauma. 4th ed.
Baltimore: Mosby; 1999:325-328,
22. BurchJM, DentonJR, Noble RD. Physiologic rationale
for abbreviated laparotomy. Surg Clin North Am.
1997;77:779-782.
23. Gould SA, Moore EE, Hoyt DB, et al. The first randomized trial of human polymerized hemoglobin as
a blood substitute in acute trauma and emergent
surgery.yy4;M Coll Surg. 2OO2;445-455.
24. Johnson JL, Moore EE, Offner PJ, et al. Resuscitation with a blood substitute abrogates pathologic
postinjury neutrophil cytotoxic function./ Trauma.
2001;50(3):449-456.
25. Biffl WL, Moore EE, Haenel JB. Hemoglobin solutions
for trauma resuscitation. In: Trunkey DD, Lewis FR,
eds. Current Therapy of Trauma. 4th ed. Baltimore:
Mosby; 1999:329-333.
26. Wilson RF, Tyburski JG, Janning SW. Sepsis in trauma.
In: Wilson RF, ed. Handbook of Trauma: Pitfalls and
Pearls. Philadelphia: Lippincott, Williams & Wilkins;
1999:596-625.
27. Jarrar D, Chaudry IH, Wang P Organ dysfunction following hemorrhage and sepsis: mechanisms and therapeutic approaches. Int f Mol Med.
1999;4(6):575-583.
28. Lee CC, Marill KA, Carter WA, Crupi RS. A current
concept of trauma-induced multiorgan failure. Ann
FmergMed. 2001;38(2):170-176.
29. Schulman C. End points of resuscitation: choosing
the right parameters to monitor. Dimens Crit Care
Nurs. 2OO2;21(1):2-I4.
30. Tatevossian R, Wo C, Velhamos G, Demetriades D,
Shoemaker W, Transcutaneous oxygen in CO2 as
early warning of tissue hypoxia and bemodynamic
shock and critically ill emergency patients, Crit Care
Med. 2000;28(7):2248-2253,
31. Mikhail J, Massive transfusion in trauma: process and
outcomes,/ Trauma Nurs. 2OO4;l l(2):55-60.