Shock Hypovolemic
Shock Hypovolemic
Shock Hypovolemic
CONTINUING EDUCATION
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
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 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
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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
/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
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Hypovolemic Shock
MONITORING DURING SHOCK AND
RESUSCITATION
OBSTRUCTIVE SHOCK
DISTRIBUTIVE SHOCK
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
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
10
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
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
11
12
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,'^
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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
14
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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
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
2005
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
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
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