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How to recognize and respond to - American Nurse Today

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How to
recognize and
respond to
HYPOVOLEMIC
SHOCK
What to do when
your patient’s
fluid volume
bottoms out
By Margaret M. Ecklund, MS, RN,
CCRN, APRN-BC, and
Christine R. Ecklund, BSN, RN
28 American Nurse Today
April 2007
ACCOMPANIED BY his daughter,
George Moran, age 81, comes to
the emergency department looking
frail and weak. His vital signs are:
blood pressure, 82/40 mm Hg;
heart rate 130 beats/minute and
regular; and oral temperature,
98.6В°F (37В° C). He weighs 125 lb
(57 kg )—5 lb (2.3 kg) less than his
normal weight. On inspection, you
detect poor skin turgor and dry
mucous membranes; on palpation,
you note his abdomen is tender but
not distended. As ordered, you obtain blood samples and send them
to the laboratory immediately.
Although Mr. Moran is lethargic,
he’s able to answer questions when
you try to obtain his history. He
states he has had nausea, vomiting,
and watery diarrhea for the last 2
days and that he fell earlier today
when getting up from a chair. His
daughter adds that several family
members have had the “stomach
flu” lately.
When laboratory results come
back, you note an elevated white
blood cell count, high blood urea
nitrogen level, and borderline-low
creatinine level (0.8). Other values
are normal. Synthesizing this information with the history and assessment findings, you begin to suspect
Mr. Moran has suffered GI tract volume loss leading to hypovolemic
shock. His shock index (heart rate
divided by systolic blood pressure)
is 1.59—significantly higher than
the normal range of 0.5 to 0.7.
Knowing that quick action is
critical, you immediately place an
18G I.V. line in Mr. Moran’s left
antecubital vein and, as ordered,
begin to infuse Ringer’s lactate at
250 ml/hour.
A perilous plunge in perfusion
Hypovolemic shock occurs when
circulatory volume drops significantly. As in other types of shock,
systemic reduction in tissue perfusion leads to decreased oxygen delivery. Unless the initial process is
reversed, prolonged oxygen deprivation causes cellular hypoxia and
metabolic waste accumulation,
leading to multisystem organ failure and death. Fortunately, early
recognition of hypovolemic shock
and aggressive treatment can dramatically improve the patient’s
outcome.
Hypovolemic shock most commonly results from blood loss. (See
Causes of hypovolemic shock.) Decreased renal function puts the elderly at higher risk for this type of
shock. Children also are at greater
risk due to their higher proportion
of body water.
Pathophysiologic process
In hypovolemia, decreased fluid
volume reduces blood return to the
heart, causing a decline in preload
(the volume of blood remaining in
the left ventricle at the end of diastole). As preload falls, cardiac output drops.
To compensate for low cardiac
output, the heart rate speeds up
and systemic vascular resistance
(SVR) increases. Increased SVR in
turn boosts cardiac output, increases tissue perfusion pressure, and
triggers catecholamine release.
Blood volume rises as interstitial
fluid shifts to the intravascular
spaces and the liver and spleen release stored red blood cells (RBCs).
These changes activate the reninangiotensin-aldosterone system,
which promotes sodium and water
retention in an effort to raise systolic pressure. Urine output then
declines. (See Correlating shock
stages with signs and symptoms.)
If blood loss continues, compensatory mechanisms maintain perfusion to vital tissues by shunting
blood away from nonvital organs.
Decreased perfusion leads to cellular injury in the catabolic state. If
the process isn’t reversed, cellular
death follows. Also, the glucose
level rises as insulin loses its ability
to control the processes triggered
by lactic acidosis. With the body in
a state of oxygen debt, anaerobic
metabolism produces lactic acid, directly reflecting poor perfusion and
oxygen debt in later shock stages.
In uncorrected hypovolemic shock,
loss of buffering ability leads to acidosis (pH below 7.35).
Assessment and diagnosis
As with Mr. Moran, the patient’s
history may provide important information. After obtaining a thorough history of the present illness,
conduct a general physical assess-
Causes of hypovolemic
shock
Hypovolemic shock most commonly
results from:
• blood loss
• trauma
• surgery with blood loss
• GI bleeding
• dehydration secondary to vomiting or diarrhea
• severe burns.
ment, including blood pressure,
pulse, temperature, oxygenation,
urine output, mental status, and
pain level.
To quickly assess fluid volume,
think of the “hose and toes” theory:
Fluid volume is sufficient if the
“hose” (kidney) is producing adequate urine and the toes are pink
in light-skinned patients or brown
in dark-skinned patients.
Expect to draw blood samples
for a complete blood count, which
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Correlating
shock stages with signs and symptoms
Signs
and Symptoms of Hypoglycemia
S
Unless treated, hypovolemic shock progresses from mild to severe, with each
stage reflecting distinct pathophysiologic conditions and exhibiting different
clinical manifestations.
Shock stage
Pathophysiology
Clinical manifestations
Mild: loss of less
than 20% (750 ml)
of blood volume
Decreased peripheral
perfusion limited to
tissues able to sustain
prolonged ischemia
(such as skin, fat, muscle,
and bone)
• Orthostatic hypotension
and tachycardia
• Cool, pale, moist skin
• Collapsed neck veins
• Concentrated urine
• Complaint of feeling cold
• With adequate compensation,
possibly no symptoms
Moderate: loss of
20% to 40% (750
to 2,000 ml) of
blood volume
Decreased perfusion of
tissues capable of
tolerating only brief
ischemic insults (such as
liver, kidneys, and gut)
• Supine hypotension and
tachycardia
• Decreased urine output
• Increased respiratory rate
• Anxiety
Severe: loss of more Decreased perfusion of
than 40% (2,000 ml) brain and heart
of blood volume
• Severe hypotension,
tachycardia, and confusion
• Decreased urine output
• Increased respiratory rate
• Anxiety
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April 2007
American Nurse Today
29
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If aggressive volume resuscitation doesn’t
improve blood pressure, vasopressors
may be given in addition to I.V. fluids.
may suggest or help rule out infection and certain other conditions.
Hemoglobin and hematocrit values
may indicate bleeding; during treatment, they provide a baseline for
gauging the patient's response to
blood transfusions or other replacement fluids. Also draw blood for
typing and screening. If the patient
has anemia with acute blood loss,
make sure blood is crossmatched.
Other useful studies may include
a liver profile, arterial blood gas
analysis, and measurement of lactic
acid, fibrinogen and fibrin split
products, and cardiac enzyme levels. Calculating the shock index
may be useful, too; in acute hypovolemia, the index rises. The physician may order an ECG to evaluate
cardiac rhythm and a chest X-ray to
look for evidence of pneumonia or
heart failure.
Management
Early intervention is crucial to a
positive outcome. Hypovolemic
shock calls for rapid volume resuscitation to restore homeostasis. Ensure the ABCs of basic resuscitation—airway, breathing, and
circulation. The underlying cause of
shock must be treated as well.
Expect to insert a large-bore
(18G or larger) peripheral I.V. line
or a central access catheter for fluid
administration; a multiple-lumen
line aids delivery of fluids and I.V.
medications. Choice of replacement
fluid depends on the type of volume lost.
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30 American Nurse Today
April 2007
Colloids and crystalloids
Colloids, whose molecules are too
large to pass through semipermeable membranes, provide volume of
higher osmolarity than crystalloids
and help prevent fluid shifts. Staying mostly within the intravascular
compartment, they maintain plasma
colloid osmotic pressure. Examples
include blood and blood products,
such as packed red blood cells
(PRBCs), whole blood, fresh frozen
plasma, hetastarch, and albumin.
If the patient has lost blood from
surgery or trauma, be prepared to
administer PRBCs, which lend oxygen-carrying capacity without
adding excessive volume. Fresh
frozen plasma helps expand intravascular volume and restore deficient clotting factors, whereas
whole blood increases volume and
boosts oxygen-carrying capacity. If
the patient has thrombocytopenia,
expect to give platelet transfusions.
Crystalloids, such as normal
saline solution and Ringer's lactate,
have smaller molecules than colloids and can penetrate semipermeable membranes. The clinician
may order 2 to 3 L of a crystalloid
to help maintain fluid and electrolyte balance. Lactated Ringer’s
solution is isotonic and provides
buffering to counteract the effects
of acidosis. Normal saline solution
is helpful for a patient who hasn’t
lost RBCs.
Because crystalloids distribute
from the intravascular space
throughout the entire extracellular
space, they must be administered
in large volumes to treat hypovolemic shock. Avoid giving
dextrose-containing crystalloids,
which may increase the serum
glucose level. (Tight glycemic
control promotes healing.)
Vasopressors aren’t a first-line
treatment for hypovolemic shock.
Normally, they cause contraction of
the peripheral vasculature, which
leads to shunting of blood to vital
organs; however, when volume is
low, this mechanism isn’t effective.
Nonetheless, if aggressive volume
resuscitation doesn’t improve blood
pressure, vasopressors may be given in addition to I.V. fluids.
Be aware that I.V. fluids increase
the patient’s risk of heart failure.
During fluid administration, be sure
to assess breath sounds, heart rate,
and oxygenation and monitor fluid
intake and output.
Other nursing interventions
Expect to administer oxygen and
ventilatory support, if needed, to
support tissue perfusion. To optimize blood pressure, position the
patient flat or in Trendelenburg’s
position to increase venous return
from the legs. But be aware that
such positioning heightens the risk
of aspiration. Hypovolemia itself
reduces gut perfusion; decreased
blood flow to the stomach can increase the risk of gastric residuals,
reflux, and aspiration. So if the
patient’s receiving enteral nutrition, discontinue tube feedings
temporarily.
Also, low perfusion puts the patient at higher risk for pressure ulcers. Although skin condition isn’t a
high priority during fluid resuscitation, you can take steps to help reduce pressure surface by obtaining
a low air-loss mattress and making
sure the patient doesn’t lie on a
moist, hard surface for extended
periods.
Complications
Unless volume is restored and
bleeding is halted, coagulopathies
may develop—and fluid resuscitation can worsen these. Hypovolemic shock also may cause other
complications, including:
• systemic infection from use of a
large-bore I.V. line for fluid resuscitation
• transfusion reaction if blood
transfusions are given
• hypothermia, which may follow
trauma, surgery, or infusion of
massive amounts of I.V. fluids.
Hypothermia may worsen acidosis, so be sure to keep the pa-
tient warm. If body temperature
drops, warm I.V. fluids externally, apply warm blankets or external warming devices, or increase
room temperature.
Promoting an optimal outcome
For a patient in hypovolemic
shock, a successful outcome hinges
largely on prompt diagnosis and
aggressive treatment. Prognosis
varies with such factors as how early treatment begins and the degree
of shock; in severe shock, death
may occur despite immediate treatment.
Elderly patients are particularly
likely to have a poor outcome. Mr.
Moran, though, was one of the
lucky ones. After 2 hours of fluid
resuscitation, his blood pressure increased, his heart rate slowed, and
his indwelling urinary catheter had
collected about 100 ml of output.
He’ll be admitted shortly to a general medical unit, where he’ll continue to receive I.V. fluids, but at a
lower rate. Thanks largely to nursing expertise and quick action, he
was able to avoid disaster.
вњЇ
Selected references
Birkhahn R, Gaeta T, Terry D, et al. Shock
index in diagnosing early acute hypovolemia. Am J Emerg Med. 2005;23:323-326.
Gaieski D, Manaker S. General evaluation
and differential diagnosis of shock in adults.
Official topic review from UpToDate. Available at: http://patients.uptodate.com/
topic.asp?file=cc_medi/11364. Accessed
March 1, 2007.
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Kelley D. Hypovolemic shock: an overview.
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888-219-5501
WaldenU.edu
Muhlberg A, Ruth-Sahd L. Treatment and interventions for hypovolemic shock secondary to hemorrhage. Dimens Crit Care Nurs.
2004;23:55-59.
Rose B, Mandel J. Treatment of severe hypovolemia or hypovolemic shock in adults.
Available at: http://patients.uptodate.com/
topic.asp?file=fldlytes/16514 . Accessed
March 1, 2007.
Margaret M. Ecklund, MS, RN, CCRN, APRN-BC, is a
Clinician VI/Nurse Practitioner in Pulmonary Medicine
at Rochester General Hospital in Rochester, N.Y.
Christine R. Ecklund, BSN, RN, is a Staff Nurse at Beth
Israel Deaconess Medical Center in Boston, Mass.
Walden University is accredited by The Higher
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April 2007
American Nurse Today
31
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