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Crit Care Nurs Q

Vol. 28, No. 1, pp. 2–19
CONTINUING EDUCATION

c 2005 Lippincott Williams & Wilkins, Inc.

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, car-
diogenic, 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 re-
suscitation 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 chal-
lenge for trauma systems and trauma cen-
enable the nurse to contribute to positive pa-
tient outcomes.
This article describes these 4 categories
ters. Rapid identification, and ensuring cor- of shock states. However, since hypovolemic
rect, aggressive treatment, are necessary for shock is the most common type of shock
patient survival. Trauma patients are at risk encountered in the trauma patient popula-
for several types of shock states: hypov- tion, the majority of the discussion will be
olemic, cardiogenic, obstructive, and distribu- dedicated to its recognition, definition, and
tive. Physiologically, regardless of the type of treatment.
shock, inadequate tissue perfusion is the re-
sult of reduced or poorly distributed blood CASE STUDY
volume. The body activates compensatory
mechanisms in an effort to improve perfu- A 35-year-old male, helmeted motorcycle
sion. Care providers must recognize and in- driver, “T-boned” a taxicab at high speed. He was
tervene rapidly to support tissue oxygenation ejected, landing on pavement 30 ft from his bike.
and blood flow; otherwise, these compen- Witnesses accessed the 911 emergency medi-
satory mechanisms will fail, resulting in a cas- cal response system; paramedics arrived quickly.
cade of events to include inflammatory re- They found the patient lying unresponsive on the
sponse, release of mediators, organ failure, pavement; respirations were agonal; pulse, weak,
and death.1 and thready; BP was unobtainable. They placed
the patient in full spinal immobilization, adminis-
The critical care nurse plays an important
tered oxygen, and supported respirations via a
role as part of the team involved in the resusci- bag, valve, mask (BVM) device. Transport time
tation and ongoing care of these patients. Un- was less than 2 minutes from the trauma center,
derstanding the underlying pathophysiology, so they elected to “scoop and haul.” Upon arrival,
recognizing signs and symptoms, and being the trauma team evaluated the patient, using Ad-
prepared to effectively respond will further vanced Trauma Life Support (ATLS) guidelines
and reported these findings upon primary survey:
Airway: patent; C spine precautions maintained
From the Scripps Mercy Hospital, San Diego, Calif. 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.

2
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Hypovolemic Shock 3

Disability: GCS 3, pupils unequal, slightly matic” shock. Initially, he suffered from ob-
reactive. structive shock as a result of tension pneu-
The patient was intubated immediately upon ar- mothorax. Further investigation revealed that
rival, using rapid sequence intubation (RSI) tech- the patient suffered from hypovolemic shock
nique. Breath sounds auscultated after intubation from pelvic fractures and internal injuries. He
was diminished, despite validation that the ET
had also suffered distributive shock secondary
tube was correctly placed. The respiratory thera-
pist reported difficulty ventilating the patient. Bilat-
to cervical and thoracic cord transection asso-
eral needle thoracostomy was performed. A right ciated with spinal column fractures. His life-
femoral vein cordis was placed, as well as inser- threatening, multisystem injuries proved chal-
tion of 2, large bore, 16-gauge, peripheral intra- lenging to sort out. However, hypovolemic
venous catheters. A clot was sent off for type and shock must always be the primary consider-
cross. Normal saline solutions were administered ation until ruled out.
intravenously; the patient remained hypotensive
and bradycardic. On secondary survey the pa- TRIMODAL DEATH PATTERN
tient was found to have the following:
Head: abrasions and scalp laceration with oc- Researchers have identified 3 major epi-
cipital skull fracture
demiological events, or trimodal patterns of
Chest: diminished breath sounds; CXR, nega-
tive for hemothorax
death from trauma. Immediate deaths, those
Abdomen: multiple contusions, distended, hy- that occur on scene shortly after injury, ac-
poactive bowel sounds count for approximately 50% of deaths due
Pelvis: unstable to compression and palpation to trauma. These usually result from cata-
GU: absent rectal tone (paralytics on board clysmic events resulting in high central ner-
from RSI); meatus WNL; prostate WNL vous system injuries, or devastating injuries
Extremities: dusky, delayed capillary refill, un- such as lacerations to the heart or major
able to palpate peripheral pulses blood vessels. Early deaths occur within sev-
Back/spine: no obvious step off eral hours and are typically the sequelae of
A foley catheter was inserted. Focused Abdo- acute hemorrhage or traumatic brain injury.
minal Sonogram for Trauma (FAST) was nega-
Late deaths may occur weeks after injury and
tive. Blood for baseline laboratory studies was
sent off, and radiological studies were ordered
are typically the result of infection or multisys-
Laboratory findings: ABG, pH 7.01; Pco2 68; tem organ failure. The preponderance of data
Po2 38; BE −13; HCO3 11.7%; O2 sat 59%; O2 demonstrates that immediate and early deaths
15 L/min 100%; INR 1.5. account for approximately 80% of trauma-
The patient remained hypotensive. Pulse var- related fatalities, with the majority as a re-
ied widely between a low of 32 and high of 120. sult of rapid exsanguination. There is a pre-
After infusion of warmed crystalloid, packed red ventable death rate associated with a failure to
blood cells and FFP, the BP stabilized at 102 sys- recognize and adequately treat patients at risk
tolic. Cardiac monitor demonstrated regular si- for acute hemorrhage. This has been reported
nus rhythm at 98. The trauma surgeon elected as high as 27%. These data suggest that the
to transport the patient, with the trauma team in
development and implementation of a strate-
attendance, to radiology for CT scan.
CT results: Closed head injury with intra-
gic approach to provide care for at-risk pa-
parenchymal contusions; C-spine fractures at tients could greatly improve outcomes. Goals
multiple levels; T-spine fractures; open book are aimed at early recognition, and adequate,
pelvic fracture, with intrapelvic blood vessel in- timely treatment to reduce the overall death
juries, multiple lower extremity fractures. rate.2

The case described above demonstrates the ROLE OF TRAUMA CENTERS

complex critical thinking processes required
by trauma team members. This patient ex- Trauma systems have been designed to get
hibited classic signs and symptoms of “trau- the “right patient, to the right resources, in
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4 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

the right time frame.” Inclusive trauma sys- pothermia, acidosis, and coagulopathy. If un-
tems assure the availability of rapid transport, resolved, shock progresses to an irreversible
by adequately trained prehospital providers, state, resulting in multisystem organ failure
to centers prepared to receive the critically in- and death.8 Others have further described
jured patients. The “right resources” and des- shock as a basic biochemical inability to prop-
tinations are typically trauma centers, which erly utilize oxygen and other nutrients, or an
are required to demonstrate rigorous physi- inappropriate or amplified stimulation of cel-
cal plant and care provider requirements. The lular signaling cascades.9
right time frame is sometimes referred to as
the “golden hour.”3 The cornerstone of this SHOCK CLASSIFICATIONS
approach is the rapid recognition and early
evaluation and treatment of severely injured Although there are a variety of definitions
patients.4 This early resuscitation phase has and methods of classification,2–9 for the pur-
typically taken place in emergency depart- poses of this discussion, shock is divided
ments; however, the resuscitation phase has into 4 pathophysiologic categories: (1) hypo-
now moved beyond the walls of the emer- volemic, (2) obstructive, (3) cardiogenic, and
gency department and now includes operat- (4) distributive. All the 4 interfere with end-
ing room resuscitation and continued aggres- organ cellular metabolism.2,10
sive resuscitation in the intensive care unit
(ICU). Therefore it is imperative that nurses in HYPOVOLEMIC SHOCK
these arenas be proficient in the recognition,
assessment, and care of the severely injured Hypovolemic shock occurs as a result of de-
trauma patient.5 creased circulating blood volume, most com-
monly from acute hemorrhage. It may also be
DEFINITION the result of fluid sequestration within the
abdominal viscera or peritoneal cavity. The
As described in the literature, there are severity of hypovolemic shock depends not
multiple definitions of shock. In the 1870s, only on the volume deficit loss, the time frame
Samuel D. Gross described shock as the “rude within which the fluid is lost, but also on the
unhinging of the machinery of life.”6 One age and preinjury health status of the individ-
hundred years later, in the 1970s, G. T. Shires ual. Clinically, hypovolemic shock is classified
discussed the severity of shock states as pro- as mild, moderate, or severe, depending on
portional to the depression in the cellular the whole blood volume loss.10
membrane potential. He proposed that shock In mild or compensated shock, less than
occurs when the physiologically regulated cir- 20% of blood volume is lost. Vasoconstric-
culation of blood fails to deliver sufficient oxy- tion begins and redistribution of blood flow
gen to sustain aerobic metabolism to the cel- is shunted to critical organs. Moderate shock
lular mitochondria. Therefore, resuscitation reflects 20% to 40% of blood volume loss;
from shock is restoration of adequate oxy- there is decreased perfusion of organs such
gen delivery to mitochondria. Organ failure, as kidneys, spleen, and pancreas. In severe
as shock sequelae, is proportional to the hy- shock, greater than 40% of blood volume is
poxic damage to intrinsic cellular function.7 lost; there is decreased perfusion of the brain
As defined by Advanced Trauma Life Support and heart. Hypovolemic shock produces com-
(ATLS), shock is the consequence of insuf- pensatory physiologic responses in almost all
ficient tissue perfusion, resulting in inade- organ systems.10
quate cellular oxygenation and an accumula-
tion of metabolic waste. The consequences of Pathophysiology of hypovolemic shock
untreated shock are metabolic derangements Hypovolemic shock usually means hem-
that result in a vicious cascade to include hy- orrhagic shock in the trauma patient. The
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Hypovolemic Shock 5

patient may be bleeding internally or exter- β-blockers are unable to mount a compen-
nally, and as a result circulating blood vol- satory tachycardia. Patients who have a con-
ume is decreased. This volume loss reduces comitant spinal cord injury cannot increase
both preload and stroke volume and causes heart rate in response to volume loss and
reduced cardiac output. hypotension due to inhibition of the sympa-
Signs and symptoms of early hypovolemic thetic nervous system.11
shock include an altered level of conscious- This catecholamine release, causing arterio-
ness, sometimes manifested in agitation and lar constriction, does not affect all systems to
restlessness, or any central nervous system the same degree. The body preserves blood
depression. Physical assessment may demon- flow to the heart and brain at the expense
strate nonspecific signs and symptoms such as of the gastrointestinal (GI) tract, the skin,
cool, clammy skin, orthostatic hypotension, and skeletal muscle. However, if the shock
mild tachycardia, and vasoconstriction.11 The state persists or worsens, myocardial func-
body is able to sustain blood pressure and tion eventually becomes impaired. The great-
tissue perfusion by employing compensatory est decrease in circulation during vasocon-
mechanisms that primarily promote vasocon- striction occurs in the visceral and splanchnic
striction to support an increase in intravascu- circulation. Intestinal perfusion is depressed
lar volume.2 out of proportion to reduction in cardiac
Late signs of shock include worsening output.10
changes in mental status to include coma, hy- Blood flow to the kidneys is preserved
potension, and marked tachycardia. It is im- with a small to moderate hemorrhage; how-
portant to know, however, that healthy adults ever, the renal vessels will constrict with
with impending hemorrhagic hypovolemic large blood loss. Eventually there is a de-
shock may not become hypotensive until as cline in glomerular filtration and urine out-
much as 30% of their circulating blood volume put. The kidneys require high blood flow
is lost.11 to maintain cellular metabolism. Sustained
hypotension may result in tubular necro-
VASOCONSTRICTION sis. Blood flow to the liver is reduced but
to a lesser extent than in peripheral tis-
Vasoconstriction is an early compensatory sue. Decreased circulation to the skin is re-
response mechanism to shock. The initial de- sponsible for the coolness associated with
crease in blood pressure inhibits the afferent hypovolemia.2
discharge of baroreceptors in the aortic arch
and carotid sinus. This stimulates sympathetic PLASMA VOLUME
nervous system output. The decrease in blood
volume inhibits the discharge of stretch re- Vasoconstriction causes a shift of fluid
ceptors in the right atrium and also stimu- between the vascular compartment and the
lates afferent discharge from chemoreceptors interstitial spaces. Normally, there is little
in the aortic arch and carotid bodies. The re- fluid movement between these 2 compart-
sulting increased sympathetic tone causes the ments. In early or compensated shock, there
release of catecholamines, epinephrine, and is a reduction in capillary hydrostatic pres-
norepinephrine, intensifying venous tone, in- sure, which allows movement of protein-free
creasing heart rate, myocardial contractility, fluid from the interstitium to the vascular
and subsequently, cardiac output. This com- space, increasing intravascular volume and
pensatory mechanism is an effort to improve decreasing interstitial volume. This extracel-
perfusion to the vital organs and tissues.2 lular fluid mobilization usually occurs over
It is important to understand, however, a 6- to 12-hour period. It is not responsible
that not all patients in hypovolemic shock for large volume changes in early phases of
demonstrate tachycardia. Patients who are on hemorrhagic shock.2
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6 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

Decreased renal blood flow activates the obic metabolism predominates, stimulating
renin-angiotensin system, stimulating produc- lactate production and subsequent metabolic
tion of angiotensin I. Angiotensin I is sub- acidosis. The resultant metabolic acidosis fur-
sequently converted to angiotensin II, a ther exacerbates the shock state, decreasing
strong vasoconstrictor that promotes aldos- sensitivity to catecholamines and stress hor-
terone release from the adrenal cortex. Si- mones, resulting in decreased myocardial con-
multaneously, angiotensin II potentiates the tractility, promoting predisposition to cardiac
action of adrenocorticotrophic hormone on dysrhythmias.2
the adrenal cortex and further promotes Lactic acidosis, the physiologic deficit re-
epinephrine release from the adrenal medulla. sulting from inadequate perfusion, is reflected
Adrenocorticotrophic hormone is released in high serum lactate levels. The amount of
from the adrenal cortex, increasing renal lactate produced correlates with total oxygen
sodium and water retention, as well as potas- debt, signifying the magnitude of hypoperfu-
sium excretion, which support the intravas- sion, the severity of shock, and also adequacy
cular volume. Simultaneously, the posterior of resuscitation. Serum lactate is considered
pituitary releases additional antidiuretic hor- a sensitive indicator of occult shock and may
mone, or vasopressin, which promotes re- be useful in patients with a significant mech-
absorption of solute-free water in the distal anism of injury yet demonstrating vital signs
tubules and collecting system of the kid- within normal limits. Since the 1960s, sev-
neys. It also further stimulates peripheral eral studies have pointed to increased death
vasoconstriction.2 rates associated with metabolic acidosis, as re-
flected in arterial pH, lactate, and base deficit
clearance.5,2 Base deficit is defined as the
CATABOLISM
amount of base, measured in millimoles, re-
quired to titrate 1 L of whole arterial blood to
During shock states, catecholamine out-
a pH value of 7.40, the sample is completely
put and glucocorticoid production create
saturated with oxygen at 37◦ C, and has a PCO2
a catabolic state. Plasma concentrations of
of 40 mm Hg.1 Base deficit is used as an index
glucagon rise. Together, catecholamines and
of the severity of shock in the adequacy of re-
glucagon promote glycogenolysis and lipoly-
suscitation, measuring global tissue acidosis.
sis. As a result, hyperglycemia, as well as ele-
Some studies suggest a correlation between
vated lactate and fatty acid levels, may be ob-
base deficit and survival probability, although
served as the shock state progresses.2
others refute this.12,13
Arterial blood gases assess acid base, ven-
ACID-BASE DISTURBANCES tilation, and oxygenation status in the in-
jured patient. Hypoxemia contributes to tis-
Acid-base disturbances are reflective of sue oxygen deficit present in hemorrhagic
the shock state. Measures of anaerobic shock; therefore, measurement of arterial
metabolism include serum bicarbonate, pH, PCO2 helps drive decision making regard-
base excess, and lactate. In compensated, ing the need for intubation and ventilatory
or mild to moderate, shock, the most fre- support.
quently observed acid-base abnormality is Treatments for metabolic acidosis are aimed
respiratory alkalosis. It is important to mon- at correcting the underlying cause: hypoper-
itor blood gases on a regular basis. Hypoxic fusion. Supporting adequate oxygen delivery
or hypotensive stimulation of the aortic and through volume loading, transfusions, and ju-
carotid chemoreceptors, the presence of dicious inotropic support are used to achieve
metabolic acidosis, and painful stimuli acti- resuscitation goals of normal values in ar-
vate the respiratory center, causing hyperven- terial pH, base deficit, lactate, and gastric
tilation. As the shock state progresses, anaer- tonometry.12,13
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Hypovolemic Shock 7

MONITORING DURING SHOCK AND OBSTRUCTIVE SHOCK

RESUSCITATION
Obstructive shock refers to a symptom com-
Frequent assessment and reassessment plex where mechanical obstruction interferes
through continuous monitoring is necessary with the ability of the heart to generate ade-
to identify and correct the causes for cir- quate cardiac output. Intravascular volume is
culatory compromise. Cardiac monitoring sufficient and the heart pumping action is ad-
should be initiated upon arrival and contin- equate. Basically, “blood can’t flow where it
ued throughout the critical care phase to needs to go.” The most frequently described
monitor and evaluate abnormalities in rate causes of obstructive shock are tension pneu-
and rhythm. Persistent tachycardia, despite mothorax, pericardial tamponade, and pul-
aggressive resuscitation efforts, may indicate monary embolus. Recall our case study. Upon
ongoing hemorrhage. Rhythm disturbances arrival to the trauma center, the patient was
may reflect a progressive shock state. On- intubated. However, the respiratory therapist
going blood pressure monitoring, pulse reported difficulty ventilating the patient, de-
oximetry, core body temperature, and urine spite the fact that correct endotracheal tube
output are all useful in assessing circulatory placement was confirmed. The trauma sur-
status. Urine output reflects renal perfusion geon performed a needle thoracostomy to re-
and indirectly, overall central perfusion. A lieve intrathoracic cavity pressure for a sus-
urine output of 1 to 2 mL/kg per hour is pected tension pneumothorax.
normal; output of less than 1 mL/kg per hour In tension pneumothorax, air accumulates
suggests inadequate resuscitation and poor in the intrathoracic cavity, causing compres-
perfusion.2 sion of the vena cava. As a result, venous re-
Central venous pressure monitoring is typ- turn to the heart is compromised, limiting car-
ically not initiated during early resuscitation, diac output. This is a life-threatening situation
but may prove useful in patients with pro- and must be corrected immediately.8
longed and extensive resuscitation, includ- In pericardial tamponade, fluid accumu-
ing massive transfusion. It may be necessary lates in the pericardial space, elevating in-
to establish central venous access in patients trapericardial pressure and impairing ventric-
where adequate peripheral intravenous (IV) ular filling. As a result, stroke volume and
access has not been successful. It is also cardiac output are reduced. As aortic pres-
an adjunctive tool to aid in the diagnosis sure falls, coronary blood flow is reduced dur-
of undefined shock or measurement of vol- ing a period of increased myocardial oxygen
ume status in patients with CHF or renal demand and, as a result, myocardial failure,
disease.2 Pulmonary artery catheter (PAC) shock, and cardiac arrest may follow.2
placement may be considered in the critical
care unit for patients suffering from undif- CARDIOGENIC SHOCK
ferentiated shock, and to guide volume re-
placement for patients with comorbid factors Cardiogenic shock is defined as the inability
such as congestive heart failure and renal of the heart to maintain adequate tissue perfu-
insufficiency. Consideration for a PAC may sion secondary to impaired pump function or
be useful in guiding resuscitation for pa- failure. In the presence of trauma, cardiogenic
tients who are not hypotensive, but exhibit shock is likely the result of an acute myocar-
more subtle signs of shock such as cool ex- dial infarction either from pretraumatic event
tremities and elevated lactate levels.14 How- or from direct myocardial injury. Cardiogenic
ever, PACs are invasive, time-consuming to in- shock could also result from transection of a
sert and maintain, and carry certain risks of coronary vessel or chamber injury after a pen-
morbidity. etrating event.2,8
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8 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

DISTRIBUTIVE SHOCK sistant to fluid administration. However, the

patient is typically bradycardic because of in-
Distributive shock describes abnormalities creased parasympathetic tone and the inhibi-
in vascular resistance, causing maldistribution tion of the sympathetic nervous system. The
of blood flow. Some of the more common team must consider the possibility of spinal
causes are sepsis, anaphylaxis, and spinal cord cord injury once hypovolemic shock is ex-
injury. cluded. However consider the major trauma
From a pathophysiologic standpoint, low patients with multisystem injuries who may
vascular resistance increases intravascular ca- be suffering from both hypovolemic shock
pacity. This expanded vascular capacity, in the and spinal cord injury. However, it is imper-
presence of a normal or low intravascular vol- ative to assume that shock in spinal cord in-
ume, causes a functional hypovolemia, result- jury patients is due to hypovolemia, and not
ing in inadequate tissue perfusion. Distribu- due to neurogenic shock. Only after blood
tive shock is also sometimes termed “warm loss is summarily ruled out, the physician
shock.” Spinal cord injury above the level should consider the diagnosis of neurogenic
of T1 results in almost unopposed parasym- shock.4,12
pathetic tone. These patients do not vaso- Diagnosis is most challenging when more
constrict and may not demonstrate the cool than one cause is present. Another example
clammy skin commonly associated with hem- is the patient who suffers a myocardial contu-
orrhagic shock. Transection of the cervical sion from blunt trauma and who also has hy-
spinal cord may impair cardiovascular con- povolemic shock from other injuries. Remem-
trol. Unopposed vagal tone contributes to the ber that many trauma patients suffer injuries
bradycardia, loss of arterial tone, and the hy- to more than one system.
potension witnessed in neurogenic shock.2,8 Drug and alcohol intoxication may also
Septic shock, resulting from infection, is make the diagnosis of hypovolemia trouble-
unusual in the early stages of acute trauma, some. Serum ethanol elevation causes the skin
except in the patient presented with grossly to be warm, flushed, and dry. Urine is usu-
contaminated wounds.4 Septic shock will be ally dilute. These patients may be hypoten-
discussed with multisystem organ failure, as it sive when supine, with exaggerated changes
is a frequent sequela of hypovolemic shock. in postural blood pressures measurements.
Hypovolemic shock victims present as cold,
DIFFERENTIAL DIAGNOSIS clammy, oliguric, and tachycardic.2,4

Shock due to hypovolemia may be confused

Treatment priorities
with, or confounded by, shock from other
causes. In some instances, there may be more Throughout every phase of trauma care,
than one type of shock in play. Consider the el- the priorities of airway, breathing, and circu-
derly patient who may have had a myocardial lation are paramount. Problems encountered
event before his car crash. Cardiogenic shock in these areas must be addressed rapidly and
produces signs and symptoms as those found sequentially. Sources of bleeding are contin-
in hypovolemia with the exception that the ually assessed. Hemodynamic monitoring is
neck veins are usually distended. However, re- performed on a continuous basis and changes
member that vein distention may not occur if reported to the trauma-attending physician.10
there is inadequate circulating fluid volume.
Hypotensive patients who sustain high FLUID RESUSCITATION
spinal cord injuries may be challenging
diagnostically. These patients will exhibit In the ICU, fluid resuscitation is carried
hypotension secondary to peripheral vasodi- out in a more controlled fashion than in the
lation. This type of shock may be relatively re- acute posttraumatic situation. During initial
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Hypovolemic Shock 9

resuscitation attempts, IV access is obtained weight. Controversy exists regarding the ap-
through the use of at least 2 large bore (14–16) propriate choice of resuscitation fluid for the
gauge or larger catheters. Femoral cordis lines trauma victim with mild to moderate hem-
are commonly used in our institution when orrhage. The focus of this controversy cen-
there are no contraindications for using this ters primarily on the effect each fluid type
site. The small ports on the pulmonary artery has on the lungs. Proponents of colloid ther-
and triple-lumen catheters are typically inade- apy argue that maintenance of the plasma col-
quate for rapid fluid resuscitation and should loid oncotic pressure (PCOP) is necessary to
be used only after other large bore catheters minimize interstitial edema, particularly in the
are in place. lungs. The concern is that massive crystalloid
resuscitation creates an oncotic pressure gra-
dient encouraging movement of fluid from
INITIAL FLUID MANAGEMENT
the intravascular space into the pulmonary
interstitium. Colloid supporters further pro-
The goal of fluid administration in the
pose that since colloids remain primarily in
trauma patient is to replace volume in or-
the intravascular space, they are more effec-
der to support cardiovascular function by in-
tive volume expanders, and also are less likely
creasing cardiac preload and to maintain ade-
to cause peripheral edema than crystalloids.
quate peripheral oxygen delivery.4 Rapid fluid
However, little support is found in the litera-
resuscitation is considered the cornerstone
ture to support superior efficacy of one solu-
of therapy by some for the initial manage-
tion over the other.2,17
ment of hypovolemic shock.2 However, there
has been controversy over the years regard-
ing the aggressive administration of IV flu-
CRYSTALLOIDS
ids to hypotensive patients with penetrating
torso wounds. Research studies from the early
Crystalloid solutions are generally safe and
1990s suggest that IV fluids should be de-
effective for resuscitation of patients in hypo-
layed until the time of definitive operative
volemic shock. Isotonic human plasma solu-
intervention.15,16
tions, with sodium as the principal osmotic
In young patients, volume infusion is typi-
active particle, are used for resuscitation.
cally infused at the maximum rate allowed by
They can be administered rapidly through pe-
the equipment and the size of the cannulated
ripheral veins due to their low viscosity. Iso-
vein until a response is appreciated. In older
tonic fluids have the same osmolality as body
patients or those with comorbid conditions
fluids; therefore, there are no osmotic forces
such as cardiac disease, fluid resuscitation is
directing fluids into, or out of, intracellular
titrated to response to avoid complications as-
compartments. During resuscitation, isotonic
sociated with hypervolemia.10
crystalloids are administered approximately
Attempting to reach normotension by the
3 to 4 times the assessed vascular deficit to
transfusion of resuscitation fluids is not nec-
account for the distribution between the in-
essarily the goal. Much time can be lost chas-
travascular and extravascular spaces. Crystal-
ing vital signs with fluid resuscitation when,
loids partition themselves in a manner simi-
in some injuries, early definitive operative in-
lar to the body’s extracellular water content:
tervention to stop blood loss is required.
75% extravascular and 25% intravascular. The
majority of complications associated with
CYSTALLOIDS VERSUS COLLOIDS the use of crystalloid solutions are either
because of undertreatment or because of
Parenteral solutions for the IV resuscitation overtreatment.2,4,17
of hypovolemic shock are classified as crys- The use of one specific crystalloid over an-
talloid or colloid, depending on molecular other is largely a matter of institutional or
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10 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

provider preference. Normal saline is the only decreased platelet count and prolongation of
crystalloid that can be mixed with blood and the partial thromboplastin time. Several com-
blood products. Patients resuscitated with plications have been associated with the use
large amounts of normal saline are at risk of dextran, to include renal failure, anaphy-
for developing hyperchloremic metabolic aci- laxis, and bleeding. Gelatins are associated
dosis because its chloride concentration is with anaphylactoid reactions. They also may
higher than that of plasma. Lactated Ringer’s cause depression of serum fibronectin. Be-
solution has the advantage of a more physio- cause of the high cost and complication rates,
logic electrolyte composition. there appears to be no clear advantage to us-
Hypertonic saline solutions are crystalloids ing colloid solutions.4,10
that contain sodium in amounts higher than
physiologic concentrations. They expand the
Blood products and component therapy
extracellular space, by creating an osmotic
effect that displaces water from the intra- Neither crystalloid or colloid solutions in-
cellular compartments. Hypertonic saline de- crease oxygen-carrying capacity. Administra-
creases wound and peripheral edema. There tion of large amounts of fluids can also prove
is some research to suggest, however, that hy- detrimental by diluting hemoglobin levels and
pertonic saline resuscitation may contribute contributing to fluid volume overload.4
to increased bleeding.2,4,10 Blood products are currently the most read-
Most sources agree that the best way to ily available fluids to increase oxygen-carrying
manage hypovolemic shock in trauma pa- capacity and cardiac preload. However, trans-
tients is the judicious use of warmed IV fluids fusions carry the risk of various blood-borne
and blood products. Many trauma centers ini- pathogens and transfusion reactions. There
tially infuse 2 to 3 L of lactated ringers or nor- is considerable debate regarding indications
mal saline and then consider blood products if for transfusion. Patients with hemorrhage of
the patient remains symptomatic. While crys- up to approximately 20% of their total blood
talloids are infusing, the blood bank has time volume can be safely volume replaced with
to type and cross-match the patient for trans- crystalloids in a ratio of 3 mL of crystalloid
fusion of type-specific blood.10,11 per milliliter of estimated blood loss. Dur-
ing the infusion of crystalloids, the blood
COLLOIDS bank has time to perform a type and cross-
match, so that, if needed, type-specific blood
Colloids are solutions that have a higher- is available for transfusion. Most agree that
molecular-weight species and create an os- patients with 20% to 40% loss of circulating
motic effect. Colloids remain in the in- blood volume, or those demonstrating evi-
travascular space for longer periods than dence of hemodynamic instability, and those
do crystalloids. Smaller quantities are re- with blood gas evidence of shock, despite ag-
quired to restore circulating blood volume. gressive fluid resuscitation, may benefit from
Colloids attract fluid from the extravascu- blood transfusions.2,8
lar to the intravascular space because of
their oncotic pressure. Examples are albumin, BLOOD TYPES AND Rh ISSUES
hetastarch, dextrans, modified fluid gelatin,
and urea bridge gelatin. They are expen- The decision to transfuse should be based
sive to use and complications have been re- on the assessment of ongoing blood loss, the
ported in their use. Albumin has been im- patient’s ability to compensate, and the avail-
plicated in decreased pulmonary function, ability of cross-matched blood products. Ad-
depressed myocardial function, decreased ditional considerations are given to the pa-
serum calcium concentration, and coagula- tient’s age and presence of comorbidities.2
tion abnormalities.10 Hetastarch may cause Ultimately, type-specific blood products are
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Hypovolemic Shock 11

preferred, but when a patient arrives in ap- that can be used in conjunction with blood
parent shock or extremis, the universal donor product transfusion. Lactated Ringer’s solu-
type O, Rh negative, is transfused using a rapid tion will cause precipitation of blood within
infusor/warmer device. the tubing.2,4,18
Rh-negative blood may be in short sup-
ply; therefore, some hospitals have poli- BLOOD COMPONENT THERAPIES
cies in place that allow Rh-positive Group
O, packed red blood cells (PRBCs) to be At this writing, component therapy remains
transfused in men, and women older than the current standard for blood transfusion.
childbearing age. The rationale behind this It refers to the utilization of the compo-
practice is that naturally occurring anti-Rh nents of whole blood to include RBCs, fresh
bodies do not exist, therefore there is no ad- frozen plasma (FFP), platelets, and cryopre-
vantage to the use of Rh-negative blood. How- cipitate. One unit of whole blood contains
ever, there is some concern that Rh-negative 200 mL of red blood cells and 250 mL of
patients may have been sensitized from preg- plasma, which contains coagulation factors.
nancy or previous transfusions and could de- Component therapy has several advantages
velop a delayed hemolytic transfusion reac- over whole blood, and evidence suggests that
tion from Rh-positive blood use. This is a rare the PRBCs and component therapy are as
occurrence; therefore, O-Rh-positive PRBCs effective as whole-blood transfusion without
are considered the first choice for emergency the disadvantages. PRBCs and components
transfusions, with consideration for the use of are more readily available and are less expen-
O-Rh-negative PRBCs for females with child- sive and easier to store than whole blood. Vol-
bearing potential.2 Some sources recommend ume expansion can be accomplished with a
that the number of transfusions of type O be combination of crystalloids and PRBCs. An-
limited to 4 units, after which type-specific other advantage of component therapy over
blood should be available in most institutions whole blood is that infusions can be tailored
receiving trauma patients. However, when specifically to the needs of the individual pa-
necessary, type O blood may be continued tient. Furthermore, PRBCs increase oxygen-
until the patient stabilizes or type specific is carrying capacity more efficiently than whole
available.2,10 blood. The disadvantage of whole blood is
Type-specific blood is ABO and Rh compat- that platelets are not well preserved, and clot-
ible and is available within less than 15 min- ting factors decrease rapidly at blood storage
utes in most institutions. Type-specific blood temperatures. For these reasons, PRBC infu-
has been shown to be safe and effective dur- sion with component therapies are consid-
ing emergency resuscitations.18 ered the methods of choice for increasing red
blood cell mass and oxygen-carrying capacity
MASSIVE TRANSFUSION in hemorrhagic shock.2

Trauma practitioners are frequently faced

with situations that require decision making COMPLICATIONS OF TRANSFUSIONS
to weigh the risks and benefits of massive
transfusions. When the decision is made to Blood-borne pathogens
proceed, there are technological considera- Improved screening has significantly
tions that affect infusion rates. Large bore decreased the incidence of blood-borne
catheters, as well as high-volume IV tubing, al- pathogens or transfusion-transmitted diseases
low for the fastest blood administration. Pres- (TTDs).2 However, they still contribute to
sure bags and/or mechanical rapid transfusion the incidence of late death from transfusion.
devices further increase flow rates. Remem- Increased awareness and concerns related
ber that normal saline is the only fluid additive to TTDs, especially HIV infection, have
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12 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

prompted caution and reconsideration of storage, the massive blood and fluid admin-
blood transfusion indications. Hepatitis B is istration further dilutes the number of cir-
the most common infectious complication. culating platelets. This dilutional thrombocy-
Before testing for hepatitis C, non-A non-B topenia causes clotting abnormalities. It is
hepatitis was the most frequent infectious important to assure that there is appropri-
complication.18 ate and timely administration of platelets and
FFP to prevent this complication. Treatment
Transfusion reactions should be based on clinical evidence of im-
paired hemostasis, by following prothrombin
Transfusion reactions are categorized into
time, partial thromboplastin time, and platelet
hemolytic and nonhemolytic types. Major
count. While circulating platelet counts of
hemolytic transfusion reactions occur as a re-
20,000 per mm3 or fewer may be adequate
sult of the interaction of antibodies in the
in nonbleeding patients, platelet transfusion
plasma of the recipient with antigens present
is appropriate for patients with evidence of
in the red cells of the donor. It is important
ongoing microvascular bleeding with levels of
to stress that the majority of hemolytic reac-
100,000 per mm3 (see references 4 and 19).
tions are due to clerical error in the identifi-
Massive transfusion therapy can contribute
cation of blood samples or in the administra-
to significant electrolyte and acid-base distur-
tion of properly cross-matched blood to the
bances. Among these are hypocalcemia, hy-
wrong patient. During high-stress situations
perkalemia, and hypokalemia. Hypocalcemia
of massive transfusion administration, metic-
occurs during massive transfusion, because
ulous attention must be paid to the processes
each unit of PRBCs contains citrate, which
surrounding blood banking and blood prod-
binds to ionized calcium in the blood. Large
uct administration to avoid this preventable
citrate doses may be toxic and can precipi-
complication.18
tate hypocalcemia. Clinical signs of hypocal-
Nonhemolytic transfusion reactions are
cemia include prolongation of the QT seg-
more common and related to reactions to
ments on ECG, skeletal muscle tremors, and
leukocytes or proteins in the donor blood.
perioral tingling. Calcium levels should be
These may be mitigated by premedication
closely monitored during massive transfu-
with antipyretics and antihistamines. Typi-
sion therapy. Citrate also may contribute
cal reactions may be mild, consisting of rash
to hypomagnesemia. Because of this re-
or mild bronchoconstriction. More rare are
lationship, treatment of hypocalcemia and
severe responses such as subglottic edema,
hypomagnesemia includes concomitant use
severe bronchoconstriction, and anaphylaxis
of calcium chloride and magnesium chlo-
with cardiovascular collapse.18
ride in massive transfusion, based on mea-
sured serum levels; empiric treatment is not
Platelet and coagulation factors recommended.2,4,7
Along with the previously mentioned con- Banked blood contains significantly ele-
cerns for blood-borne pathogens and trans- vated potassium levels because of cell lysis
fusion reactions, there are several other that occurs during the collection and stor-
complications related to blood product trans- age of blood. Hyperkalemia, however, is rare
fusions, with higher complications rates asso- during massive transfusion, because packed
ciated with massive transfusion therapy, often cells quickly reestablish their ionic pump-
considered 10 U or more. Massive transfusion ing mechanism and potassium is rapidly ab-
of blood products and concurrent infusion of sorbed. In actuality, hypokalemia occurs more
large volumes of crystalloid cause certain frequently secondary to transient metabolic
hematologic and physiologic consequences. alkalosis occurring during massive transfu-
Not only do coagulation factors and platelet sion, which causes potassium to move into
numbers and function diminish during RBC the cells.2,4,7
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Hypovolemic Shock 13

Acid-base disorders are commonly associ- fusions, and exposure of body cavities during
ated with large volume transfusions. Even surgery.5
though banked blood is acidic because of its Gentilello classifies hypothermia in trauma
citrate content, metabolic acidosis is not typi- patients into 3 risk categories based on core
cally a result of the transfusions, but is related body temperature. Mild hypothermia (34◦ C–
to underlying hypovolemic shock. Treatment 36◦ C) accelerates oxygen consumption in
should concentrate on improving tissue per- an at-risk patient population. Moderate hy-
fusion and oxygenation as well as an ongoing pothermia (32◦ C–34◦ C) further slows physio-
search for underlying sources of hemorrhage. logic functions. Severe hypothermia (<32◦ C)
Sodium bicarbonate administration is not rec- is considered a life-threatening emergency.21
ommended and has several detrimental side There are a number of adverse clinical ef-
effects. In rare circumstances, a trauma pa- fects related to hypothermia. These are car-
tient may have metabolic acidosis due to a diac dysrhythmias, reduction in cardiac out-
cause other than hypovolemia, such as comor- put, increasing systemic vascular resistance,
bid factors to include diabetic ketoacidosis, increased lactic acid production, and coagu-
carbon monoxide (CO) poisoning, drug, or lopathic bleeding. Hypothermia has a deleteri-
toxic ingestion.2 ous effect on the oxyhemoglobin dissociation
curve, shifting it to the left, which impairs
HYPOTHERMIA oxygen delivery and worsens the shock
state.7,10
Hypothermia is a serious consequence Many research studies have directly linked
of massive blood product transfusion. Pro- the presence of hypothermia in trauma pa-
gressive core hypothermia with persistent tients with high mortality rates.19–21 The pri-
metabolic acidosis is the precursor of se- mary goal is to identify those patients at risk
vere and ongoing coagulopathy states.5 There and to intervene in this cycle of hypothermia,
are complex pathophysiologic interactions acidosis, and coagulopathy.5 Core tempera-
at play that contribute to impaired coagula- ture should be monitored continuously. At our
tion. Mikhail refers to the physiologic lim- institution we use a foley catheter with a ther-
its of the body in response to hypovolemic mal measuring device that provides contin-
shock as “the trauma triad of death”; hy- uous core temperature measurement. Efforts
pothermia, acidosis, and coagulopathy.5 Hy- to prevent hypothermia should be employed
pothermia has been strongly implicated in such as using a high-volume fluid warmer dur-
the development of acidosis and is frequently ing massive transfusion therapy.
demonstrated as a consequence of severe in- Based on these findings, the surgical ap-
jury and routinely prescribed resuscitation proach to the care of the severely injured
efforts.5,7 Studies suggest that as many as two trauma patient has changed over time. Early
thirds of all trauma patients arrive at emer- on, the goal of trauma surgeons was to pro-
gency departments with hypothermia, regard- vide definitive operative intervention by per-
less of geographic locale.20 Many trauma pa- forming a traditional exploratory laparotomy,
tients develop hypothermia at some point where all injuries were identified and re-
in their treatment and this is poorly toler- paired. Patients would spend long periods
ated. Hypothermia occurs in trauma patients of time in the operating room, receiving flu-
with minimal cold stress secondary to in- ids, blood products, and with open peri-
adequate tissue oxygenation and perfusion, toneum, resulting in core thermal tempera-
preventing the body from generating enough ture loss. Predictable evaporative heat loss
heat to maintain normothermia.21 Predispos- with an open peritoneum, despite state-of-
ing factors are age, injury severity, impaired the-art resuscitation procedures, is 4.6◦ C per
thermogenesis, elevated serum alcohol lev- hour.22 Patients would leave the operating
els, fluid resuscitation, blood product trans- room cold and coagulopathic. Currently the
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14 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

goal in trauma operative resuscitation is to Active core rewarming techniques include

perform “damage control” or staged laparo- the administration of warmed humidified air,
tomy. This initial procedure is abbreviated heated body cavity lavage to include peri-
and intended to control hemorrhage and con- toneum and pleura, and warmed IV fluid
tamination, pack the abdomen, perform tem- infusion and blood transfusions. Patients re-
porary closure of the abdominal wall, and quiring large boluses of fluid for resuscita-
move the patient quickly to the ICU for fur- tion as well as blood products can receive a
ther stabilization and rewarming procedures. substantial amount of heat through warm IV
Stopping or abbreviating the initial procedure fluids.
allows the trauma team to correct coagu- Extracorporeal circulatory rewarming tech-
lopathy, maximize oxygen delivery, and re- niques, such as cardiopulmonary bypass,
verse acidosis and hypothermia. Following venovenous, or arteriovenous, are the most ef-
stabilization in the ICU, the patient can re- ficient rewarming methods. However, they re-
turn to the operating room for a more con- quire large bore vessel cannulation, especially
trolled completion of the surgical procedure.7 trained technician and dedication to the duty.
Again, the goal is to prevent the triad of hy- Therefore, these procedures are typically re-
pothermia, acidosis, and coagulopathy, be- stricted to a few tertiary centers.21
cause of the high mortality associated with
this syndrome.5 As we compress the time
frames through which we move our patients Coagulopathy
toward definitive operative intervention, it Coagulopathy, or hypocoagulability after
is imperative that critical care nurses un- major trauma, is common in severely injured
derstand their role in intervening in this patients and recognized as a major cause
pathogenesis. of early death. There are many contribut-
ing factors, and the pathophysiologic rela-
tionships are complex. Little progress has
Rewarming techniques been made in correcting this phenomenon
The selection of rewarming techniques is once it develops. Virtually all normal physi-
based on how severely hypothermia is affect- ologic clotting mechanisms are severely de-
ing the patient. Stable patients who are mildly ranged in the cold, acidotic, bleeding trauma
hypothermic, and without life-threatening in- patient. The clotting cascade, governed by
juries, are typically treated with passive exter- a series of temperature sensitive reactions,
nal rewarming techniques. Passive rewarming is inhibited during episodes of hypothermia.
techniques involve removing wet clothing, in- Clotting abnormalities are exacerbated when
creasing ambient room temperature, decreas- core body temperature falls below 34◦ C.
ing airflow and insulating the patient, and al- Platelet function is also affected by low body
lowing his or her metabolic heat to increase temperatures.
body temperature. Treatment for hypovolemia includes infu-
Active external rewarming techniques in- sion of cystalloids and blood products. Coag-
clude warm fluid circulating, convection air, ulopathy becomes clinically important during
“space blankets,” and radiant heat lamps. massive transfusion therapy. Coagulation fac-
Head covering is important, as 50% of radi- tors are rapidly depleted. During shock, hep-
ant heat loss occurs from the scalp. These atic function is impaired, impacting the ability
strategies are typically more effective in pre- of the liver to rapidly mobilize additional coag-
venting hypothermia than in treating it. It ulation factors. Prothrombin time and partial
should not be the sole source of rewarming thromboplastin time should be carefully mon-
for patients exhibiting an adverse response to itored. Transfusion of FFP and platelets should
hypothermia, as results are not immediately be administered on the basis of the results of
effective. coagulation profiles.4
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Hypovolemic Shock 15

BLOOD SUBSTITUTES istration has approved transfusion of up to

10 consecutive units of polytteme for acute
Despite advances in detecting TTDs, con- bleeding. Stage 3 clinical trials are currently
cerns still remain regarding the risk of in process in several trauma centers.
transmitting hepatitis and human immun-
odeficiency virus (HIV) during transfusion SHOCK SEQUELAE
therapy. There are reports of PRBC count
shortages every year, and storage of red blood Systemic inflammatory response
cells has finite limitations. As a result, there syndrome
is a great deal of interest in the development Systemic inflammatory response syndrome
of blood substitutes as an alternative choice (SIRS) describes the pathophysiologic re-
in the treatment of hypovolemic shock. Un- sponse to a cascade of events precipitated
like blood, hemoglobin substitutes require by shock. Usually after trauma, a controlled
no cross-match, have a long shelf life, and inflammatory response occurs, which is de-
reportedly carry no risk of blood-borne vi- signed to heal wounds and ward off infection.
ral pathogens. Additionally, since they have However, continuous stimulation or severe in-
a lower viscosity than blood, flow through fection may result in a sustained inflammation
small capillaries may be enhanced, which po- (SIRS). The result is an imbalance of cellular
tentiates peripheral oxygen delivery.4,23 Pre- oxygen supply and demand, which results in
clinical studies showed hemoglobin substi- oxygen extraction deficit. This inflammatory
tutes to be as effective as blood and more response may occur without any source of
effective than standard colloid or crystalloid bacterial infection.9
solutions for resuscitation from hemorrhagic Overwhelming SIRS occurs with persistent
and septic shock. The hope was to provide stimulation disrupting anaerobic cellular cy-
an immediate on-site replacement for trau- cles. Disruption in the process of cellular
matic blood loss, prevent tissue ischemia and metabolism promotes a cascade of events in-
organ failure, and provide effective hemo- cluding promotion of adhesion of molecules,
dynamic support for septic-shock–induced catecholamines, chemotaxis, and a coagula-
hypotension.23,24 tion cascade. There is an accompanying de-
Recent research supports the concept that crease in vascular resistance resulting in pro-
postinjury multiple organ failure is related found increased cardiac index, designed to
to inflammatory response. Biologic media- promote oxygen delivery and cellular oxy-
tors present in stored blood have been im- gen uptake. This hypermetabolic demand,
plicated in early postinjury hyperinflamma- coupled with acute deficit in oxygen ex-
tory syndrome and multiple organ failure traction and metabolic failure, is precur-
through priming of circulating neutrophils. sors of multiple organ dysfunction syndrome
Some newer hemoglobin-based substitutes (MODS).9
are free of priming agents and may pro-
vide an alternative to transfusing PRBCs in
the early postinjury phase.22,24,25 Human- MODS
polymerized hemoglobin (PolyHeme C ) is a Historically, infection has been considered
universally compatible, pathogen-free, read- the cause of SIRS and MODS. Typical sources
ily available, oxygen-carrying blood substitute of infection are IV catheters placed in the pre-
being developed for use in case of urgent hospital environment or emergency depart-
blood loss. Recent study shows that this com- ment. Also implicated are urethral catheters
pound increases survival in patients with life- and endotracheal tubes. Decreased gastric
threatening red blood cell levels by maintain- acid allows for increased numbers of bac-
ing hemoglobin levels in the absence of red teria to survive and multiply, theoretically,
cell transfusion.23 The Food and Drug Admin- allowing translocation of bacteria in the
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16 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

distal bowel, theoretically resulting in high the mortality rate climbs as high as 80% to
pneumonia rates.26 100%.10
Studies show that approximately 60% of
trauma patients will have clinical signs of
sepsis without an apparent bacterial source. End points of resuscitation
Sepsis, and the ensuing multiple organ fail- At what point does one determine that re-
ure, remains a leading cause of death in suscitation is complete? Many researchers use
the surgical ICU, despite significant advances the same clinical, physiologic, or laboratory
made regarding the management of trauma studies to identify subtle hypoperfusion and
victims.27 Sepsis is characterized by increased to determine when adequate or normal perfu-
oxygen consumption, and increased car- sion resumes following resuscitation. Typical
diac index with decreased vascular resis- end points are blood pressure, heart rate, and
tance. These are indicators of the hyperdy- urine output.14 However, recent studies sug-
namic cardiovascular state associated with gest tissue hypoperfusion can persist despite
sepsis.9 normal vital signs. Cardiac and pulmonary
The process of an uncontrolled inflamma- function can be monitored fairly accurately in
tory response with a progression to MODS the ICU with current technology. By contrast,
is recognized as a defect in cellular signal- tissue perfusion, which represents circulatory
ing. Recall the previous discussion of trimodal function of the peripheral tissues, is measured
death patterns following major traumatic in- indirectly by a variety of subjective symptoms,
jury. Late deaths may occur 3 to 4 weeks af- such as vital signs, pulse rate and quality, skin
ter the initial shock episode. Inadequate early temperature, color, and moistness as well as
resuscitation has been implicated in the cas- mental status. These assessments are routinely
cade of acidosis, hypothermia, and coagu- used to infer circulatory status and tissue per-
lopathy. This triad leads to multisystem or- fusion, but they are not direct quantitative
gan failure and death. Lee and others describe measurements of tissue perfusion.29 The chal-
the initial response to shock and develop- lenge is to identify those patients at risk for
ment of SIRS, followed by progressive organ hypoperfusion; it may be present despite nor-
failure. This continuum is initiated and per- mal cardiac indices.14 Other modes of assess-
petuated by inflammation and inflammatory ment, to include gastric tonometry, transcu-
mediators.28 taneous oxygen, and CO2 measurements, are
These topics are complex, requiring in- currently being utilized as early warning signs
depth discussion and, as such, are beyond the of tissue hypoxia and hemodynamic shock in
scope of this overview article. However, it is critically ill patients.30
important for the critical care nurse to ex- If we go back and review the definition
plore ongoing research regarding cytokines, of shock as the consequence of insufficient
complement activation, and lipid mediators. tissue perfusion, resulting in inadequate cel-
Studies are currently adding to the body of lular oxygenation, what parameters do we
knowledge regarding inflammatory response choose to measure cellular oxygenation and
and multisystem organ failure after hypov- tissue perfusion? In patients with inadequate
olemic shock. tissue perfusion, oxygen delivery is insuffi-
As compensatory mechanisms continue to cient for the generation of adenosine triphos-
fail, tissue ischemia results from hypoperfu- phate. Without adenosine triphosphate, the
sion as blood flow is shunted away from tis- body cannot sustain normal cellular func-
sues with high metabolic demands, either tion. Anaerobic metabolism and tissue aci-
from microvascular injury or from inflamma- dosis are results. CO2 levels increase in the
tory response. Organ system failures com- splanchnic or gut circulation. Successful re-
monly seen are pulmonary, hepatic, and renal suscitation from shock is measured by a lim-
failure. When 3 or more systems are affected, itation of oxygen debt and tissue acidosis
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Hypovolemic Shock 17

with the return of aerobic metabolism.29,30 requiring aggressive resuscitation will demon-
Clinicians rely upon both global and organ- strate abnormally low values because of ei-
specific parameters to measure end products ther inadequate oxygen delivery or excessive
of inotropic metabolism to determine if com- oxygen demand by the tissues. Normal val-
plete resuscitation has been achieved. Basi- ues for SvO2 are between 65% and 80%; when
cally, global indexes measure overall degree of values fall below 50%, anaerobic metabolism
hypoperfusion, based on a number of readily is present. A low VO2 tells us that the pa-
available data sets. Some of these include the tient is underresuscitated, or still in shock, but
following. it is nonspecific as to the cause. This tech-
nology requires invasive monitoring via a PA
catheter, which is associated with significant
Oxygen delivery index morbidity to include improper catheter place-
Oxygen delivery index (DO2 I) (normal ment, pneumothorax, infection, and equip-
value 500–600 mL/min/m2 ) is determined by ment malfunction.29
CO (carbon monoxide), hemoglobin satura-
tion, and the ability of the lungs to load oxy-
gen onto the hemoglobin molecule. In severe Arteriovenous carbon dioxide gradient
hemorrhagic shock, there is a decrease in cir- The gradient between arterial and mixed
culating hemoglobin, which influences this venous PACO2 levels reflects the degree and
component of oxygen delivery. duration of hypoperfusion and is an excel-
Cardiac output is affected by several clinical lent barometer of the degree of hypovolemic
conditions related to trauma, to include acute shock. Normally, CO2 is cleared in the pul-
myocardial infarction, hypovolemia, septic monary circulation, but in profound shock
shock, neurogenic shock, cardiac contusion, there is a decrease in cardiac output and poor
and pericardial tamponade. pulmonary blood flow, resulting in an accu-
Pulmonary function relative to oxygen mulation of PACO2 in the tissues. A gap greater
delivery is affected by the presence of than 11 mm Hg suggests severe compromise.
pneumothorax, hemothorax, flail chest, pul- While arteriovenous carbon dioxide gradient
monary contusion, loss of effective airway, in- (AVPACO2 ) provides a general assessment re-
adequate mechanical ventilation, and other garding the effectiveness of resuscitation ef-
sequelae of trauma, to include pneumonia, forts, it does not provide specific organic
atelectasis, excessive secretions, and patient information.29
positioning. In a severely injured patient, it There have been recent technological ad-
is common to exhibit abnormal DO2 I val- vances that may provide more informa-
ues based on any, or all, of these clinical tion regarding organ-specific or regional
factors. resuscitation effectiveness. These are tonom-
The oxygen consumption index value etry, capnometry, and near-infrared spec-
(normal value, 125 mL/min/m2 ) may mea- troscopy. We will discuss their use in mea-
sure 4 or 5 times the norm in a critically suring specific intracellular tissue response to
injured patient. Some causes of increased resuscitation.
VO2 I include pain, agitation, posturing,
fever, increased work of breathing, and
tachycardia. Gastric tonometry
Gastric tonometry assesses gastric mucosal
pH as a marker of the adequacy of resusci-
Mixed venous oxygen saturation tation, evaluating perfusion at the splanch-
Continuous mixed venous oxygen satura- nic bed. The GI tract is very sensitive to
tion (SvO2 ) monitoring reflects how much any decrease in circulating volume and may
oxygen was consumed by the tissues. Patients significantly compromise gut perfusion. This
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18 CRITICAL CARE NURSING QUARTERLY/JANUARY–MARCH 2005

technique involves the use of a nasogastric in predicting patients at risk for multisys-
tube with a saline-filled, gas-permeable sili- tem organ failure early in the course of
cone balloon at the tip to measure CO2 emit- resuscitation.
ted from the gastric cells. PACO2 is then con- Both global parameter management such
verted to a pH value. A pH value less than 7.35 as SvO2 , lactate, and base deficit are helpful
suggests anaerobic metabolism, a potentially in determining decompensation or improve-
negative predictor of adequate splanchnic ment in resuscitation states. Care providers
perfusion, raising the patient’s risk for MODS should not be lulled into a false sense
and sepsis. Studies however are not conclu- of security, when vital signs and basic
sive, yet there are indications that gastric hemodynamic parameters fall within nor-
tonometry warrants consideration as a use- mal limits during resuscitation. New tech-
ful assessment tool in measuring gastric tissue nologies measuring regional tissue perfusion
perfusion.29 may be an adjunct tool in this assessment
process.29

Sublingual capnometry SUMMARY

Recent research involving both animal and
human subjects suggests that measurement of Shock is a complex physiologic state, re-
the proximal GI tract using sublingual PACO2 sulting in extreme dysfunction of cellular bio-
strongly correlates with decreases in distal gut chemistry, resulting inadequate tissue perfu-
blood flow and increases in lactic acid dur- sion, and cellular death. Hypovolemic shock
ing shock states. Since it is a relatively simple, is most commonly seen in major trauma pa-
noninvasive procedure, it has potential as an tients, although the major trauma victim is ad-
early triage resuscitation tool.29 A microelec- ditionally at risk for cardiogenic, obstructive,
trode CO2 probe is placed under the tongue, and distributive shock. Differential diagnoses
providing continuous information regarding can be complex.
tissue perfusion of the proximal GI tract. Con- Resuscitation from shock is restoration
tinued research is necessary, but early indica- of adequate tissue perfusion. Early identi-
tors are promising. fication and aggressive treatment is neces-
sary to prevent or mitigate the effects of
shock states, SIRS and MODS. Current ther-
Near-infrared spectroscopy apies are not without controversy. Ongoing
Near-infrared spectroscopy is another tech- research is aimed at further understand-
nology on the horizon that may show promise ing the complex biochemical and physi-
as a guide to end points of resuscitation. ologic responses to shock, to guide fur-
Minimally invasive, it measures intracellular ther development of appropriate treatment
oxygen levels, quantifies intracellular func- methodologies.
tion, and identifies other conditions that The critical care nurse remains a key mem-
may affect intracellular metabolism.29 It as- ber of the trauma team as resuscitation mea-
sesses the absorption of infrared light by satu- sures are continued into the critical care en-
rated hemoglobin molecules and cytochrome- vironment. It is imperative that the critical
a,a3 . It works by passing light waves via care nurse understand the trauma patient’s
probes through muscle tissue. The device complex physiologic response to injury, be
displays levels of saturated hemoglobin and familiar with methods to monitor for key
cytochrome-a,a3 to alert providers to organ- indicators of shock states, and respond as
specific hypoxia or to indicate successful a team member to provide timely and ag-
resuscitation efforts through the reappear- gressive treatment to achieve positive patient
ance of reflected red light. It holds promise outcomes.
LWW/CCNQ lwwj015-03 January 5, 2005 15:15 Char Count=

Hypovolemic Shock 19

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