Upon completion of this
course the student will be able to:
Define Hypovolemic Shock
Describe the difference
between compensated, uncompensated and irreversible Hypovolemic Shock
Discuss the classes of
hemorrhage
List two fluid based
treatment options
Explain the role that
vasopressors play in treatment of Hypovolemic Shock
Hypovolemic
Shock Hypovolemic
shock refers to a medical or surgical condition in which rapid fluid
loss results in multiple organ failure due to inadequate perfusion.
Most often, hypovolemic shock is secondary to rapid blood loss
(hemorrhagic shock). It is defined as approximately 1 Liter or 1/5 loss
of circulating volume). The following is the sequence of events that
under perfused tissue goes through:
Profound ischemia for
unperfused tissue causes a switch to anaerobic metabolism
Which leads to Lactic
Acid waste
This causes decreased
ATP to be available for cell work
The cell membrane
cannot function and it dies
This causes release of
intracellular enzymes and inflammatory mediators
This inflammatory
process wrecks havoc on the Lungs, Kidneys, Digestive Tract, Capillary
Lining and Coagulation. Whew!
There
are 3 Stages in Hypovolemic Shock: Compensated, Uncompensated and
Irreversible:
Compensated
– The body is still able to compensate for the decrease in
perfusion. Cardiac Output and systolic blood pressure are maintained.
Uncompensated –
The body’s compensation mechanisms are starting to fail.
Blood pressure begins to decrease and patient condition worsens.
Irreversible
– Cell and tissue ischemia leads to organ death due to lack
of perfusion. This process may begin on day one and continue to occur
for up to three weeks after the initial insult. Under such
circumstances, the patient should be re-evaluated to determine whether
some reversible causes of the persistent shock may have been
overlooked.
Treatable
Causes of Hypovolemic Shock: Hemorrhage
Laceration of a vein or
artery
Open wounds
Fractured pelvis (may
be associated with 1500cc blood loss)
Fractured femur (may be
associated with 500-1000cc blood loss)
Upper/Lower GI Bleed
Pnuemo/Hemothorax
Saline
or Combined Saline/Water Loss
Gastrointestinal losses
(vomiting, diarrhea)
High Fever
Excessive sweating
Diuretics
Third
Spacing (Fluid shifts):
Soft tissue trauma
Sepsis
Peritonitis (intestinal
obstruction)
Ascites
Burn injuries
Other
causes of hypovolemic shock include:
Inadequate fluid
administration (even if the patient clinically appears to be overloaded
with fluid)
Inadequate ventilation
or oxygenation
Adrenal insufficiency
Hypothermia
Hypocalcemia
Classes
of Hemorrhage
Classes
of hemorrhage have been defined, based on the percentage of blood
volume loss. However, the distinction between these classes in the
hypovolemic patient often is less apparent. Treatment should be
aggressive and directed more by response to therapy than by initial
classification.
Class
I hemorrhage (loss of 0-15%)
In the absence of
complications, only minimal tachycardia is seen.
Usually, no changes in
BP, pulse pressure, or respiratory rate occur.
A delay in capillary
refill of longer than 3 seconds corresponds to a volume loss of
approximately 10%.
Class
II hemorrhage (loss of 15-30%)
Clinical symptoms
include tachycardia (rate >100 beats per minute), tachypnea,
decrease in pulse pressure, cool clammy skin, delayed capillary refill,
and slight anxiety.
The decrease in pulse
pressure is a result of increased catecholamine levels, which causes
increase in peripheral vascular resistance and a subsequent increase in
the diastolic BP.
Class
III hemorrhage (loss of 30-40%)
By this point, patients
usually have marked tachypnea and tachycardia, decreased systolic BP,
oliguria, and significant changes in mental status, such as confusion
or agitation.
In patients without
other injuries or fluid losses, 30-40% is the smallest amount of blood
loss that consistently causes a decrease in systolic BP.
Most of these patients
require blood transfusions, but the decision to administer blood should
be based on the initial response to fluids.
Class
IV hemorrhage (loss of >40%)
Symptoms include the
following: marked tachycardia decreased systolic BP, narrowed pulse
pressure (or immeasurable diastolic pressure), and markedly decreased
(or no) urinary output, depressed mental status (or loss of
consciousness), and cold and pale skin.
This amount of
hemorrhage is immediately life threatening.
Note:
In the patient with trauma, hemorrhage usually is the presumed cause of
shock. Treatment The
initial resuscitative effort is to attempt to correct the absolute and
relative hypovolemia by refilling the vascular tree. There is good
evidence that early goal directed aggressive volume resuscitation
improves outcomes in hypovolemic shock. Because resuscitation efforts
are not always black and white, treatment must be individualized for
patient condition and need. The following are broad guidelines for the
treatment of hypovolemic shock:
Targeting O2 delivery
to vital organs rather then a specific B/P or heart rate
PA catheter is not
necessarily a mainstay but can offer a more detailed view of patient
condition. If PA catheter not available, try using CVP monitoring for
baseline.
PiCCO catheter, this is
a catheter that is placed in the femoral artery that provides
information about hemodynamic stability by measuring heart and lung
volumes rather then pressure.
Fluid
Replacement Choices Conventional
“crystal”loids
(see through) include both balanced salt solutions (BSS) and hypotonic
salt solutions. Balanced salt solutions include such fluids as 0.9%
NaCl (normal saline), and Ringer's Lactate solutions. These solutions
are characterized by having an electrolyte composition or calculated
osmolality approximating that of plasma (isotonic). Balanced salt
solutions distribute approximately ¾ or their volume to the
extravascular space with ¼ of the volume remaining in the
intravascular space.
Colloid solutions
are solutions of proteins, starches, dextrans, and gelatins containing
molecules sufficiently large enough so that they do not normally cross
capillary membranes. Under normal conditions most of the administered
volume remains in the intravascular space (unless tissue is damaged and
then it can cross membranes). Once colloids have leaked into the
interstitium, they must be removed by the lymphatic system or they will
exert a reverse pressure gradient, drawing water from the vascular
space. The removal of colloids from the interstitium is typically much
slower than that of crystalloids.
Blood
Component Therapy
Packed Red Blood Cells
- Red cell transfusions initially may be achieved with uncross-matched
type O red cells. If a patient’s blood type has been
determined, ABO and Rh specific red cells can be used. Every effort
should be made to establish the blood type of a patient prior to
transfusion to preserve type O red cell availability and accurately
determine the patient’s blood type.
Platelets - Platelet
transfusion therapy after massive transfusion is an accepted
intervention in the presence of micro-vascular bleeding prior to
documentation of thrombocytopenia. The platelet transfusion dose
recommended is 1 unit per 10 kg body weight for platelet counts
<50,000 or when platelet dysfunction is suspected.
Plasma –
Plasma (FFP) transfusion therapy should be instituted after laboratory
confirmation of coagulation factor deficiencies. The recommended dose
is 10-15 mL/kg body weight for PT/PTT>1.5 normal range.
Cryoprecipitate -
Cryoprecipitate therapy should be instituted for the correction of
laboratory evidence of hypo-fibrinogenemia (fibrinogen <100
mg/dl). Dosing will depend on the degree of hypo-fibrinogenemia and the
patient’s weight. For an average size adult, 6-unit pool for
fibrinogen levels between 50-100 mg/dl and 12-unit pool for fibrinogen
levels <50 mg/dl.
Re-establishing
Circulation In
addition to fluid resuscitative measures, the use of vasopressors may
be required to assist with the restoration of circulation. Vasopressors
are agents that cause constriction of blood vessels, leading to an
increase in blood pressure. Some vasopressors are also positive
inotropes (capable of increasing contractility of the heart) and/or
positive chronotropes (capable of increasing heart rate). The
hemodynamic effects of most vasopressors occurs secondary to their
interactions with receptors in the heart and vascular system. The
following vasopressors should be considered to improve circulatory
efforts in hypovolemic shock:
Norepinephrine Norepinephrine
is one of the principal neurotransmitters chemical substances involved
in the transmission of nerve impulses in the sympathetic nervous
system. It is released from nerve cells, and is indicated for the
treatment of acute hypotension resulting from conditions such as spinal
anesthesia, myocardial infarction, septicemia, blood transfusions, and
drug reactions. This agent is also used adjunctively in the treatment
of cardiac arrest and profound hypotension. Norepinephrine is a potent
alpha adrenoceptor agonist and is therefore a strong vasoconstrictor,
increasing systolic and diastolic blood pressures. In addition,
Norepinephrine stimulates beta 1 cells so it increases both heart rate
and contractility.
Epinephrine Epinephrine
is another neurotransmitter in the sympathetic nervous system, but it
is not released from nerve cells; rather, epinephrine is a hormone
secreted by the adrenal medulla. Epinephrine is used intravenously
during advanced cardiac life support and may also be used to treat
other conditions, including anaphylactic shock and acute, severe asthma
unresponsive to normal treatment. Because Epinephrine is a potent alpha
and beta adrenoceptor agonist, it is also a powerful vasoconstrictor
with both positive inotropic, and chronotropic effects. Epinephrine
causes increased heart rate, increased force of contraction, an
increase in cardiac output, and increased systolic blood pressure. The
vasoconstrictive effects of epinephrine become more apparent as the
dose is increased.
Dopamine Dopamine,
a precursor of norepinephrine and epinephrine, is also a
neurotransmitter. Dopamine is found in both the central and peripheral
nervous systems and is released from nerve cells. Dopamine is indicated
in the treatment of shock due to myocardial infarction, trauma,
septicemia, open-heart surgery, renal failure, and chronic cardiac
decompensation. The effects of Dopamine are complex and dose dependent.
Dopamine directly stimulates dopaminergic receptors, alpha and beta
adrenoceptors, and it indirectly causes the release of endogenous
norepinephrine. At low doses (l to 5mcg/kg/minute), dopamine directly
stimulates dopaminergic receptors on arteries in the kidneys, abdomen,
heart, and brain and causes vasodilatation. At these doses, urine
output may increase, but blood pressure and heart rate are usually not
affected. As the dose is increased (5 to 10 mcg/kg/min), dopamine
stimulates beta 1 adrenoceptors, resulting in positive inotropic and
chronotropic effects, which increases myocardial contractility, and
heart rate, which results in, enhanced cardiac output. At higher doses
(greater than 10 mcg/kg/min), dopamine exerts effects primarily
alpha-receptors, and extensive vasoconstriction causes blood pressure
to increase.
Phenylephrine
(Neosynephrine) Phenylephrine
is chemically related to epinephrine and used to treat hypotension
resulting from shock, shock like states, anesthesia, or
hypersensitivity reactions to drugs.
Phenylephrine
is a powerful vasoconstrictor that strongly stimulates alpha
adrenoceptors but has little effect on the beta adrenoceptors of the
heart. Its vasoconstrictive properties are similar to those of
norepinephrine. Phenylephrine increases systolic and diastolic blood
pressures in a dose dependent manner, but because it has minimal
effects on beta-receptors, heart rate and contractility are generally
not affected.
Vasopressin Vasopressin
is a unique vasopressor for two reasons. First, its principal use is
for a condition unrelated to its vasopressor properties. Vasopressin is
an antidiuretic hormone indicated to inhibit diuresis in patients with
diabetes insipidus. However, at higher doses, vasopressin causes
vasoconstriction. Because there is a fair amount of evidence to support
its effectiveness as a vasopressor, vasopressin is now considered as an
alternative to epinephrine for the treatment of adult shock-refractory
ventricular fibrillation during advanced cardiac life support.
Vasopressin is a distinctive vasopressor also because its
vasoconstrictive effects do not result from its interaction with
adrenoceptors; rather, vasoconstriction arises from vasopressin's
actions on vasopressin receptors. Vasopressin receptors are classified
as V-1 and V-2 receptors. V-1 receptors are located on arterial smooth
muscle, and V-2 receptors are found in renal tubules. It is
Vasopressin's interaction with V-1 receptors that is responsible for
its potent vasopressor effects.
References
Disorders of fluid and
electrolyte balance: The basics. (June 2003). Retrieved on December 25,
2003 at: www.members.tripod.com/~lyser/ivfs.html Heitz,
U., & Horne, M., M. (2005). Fluid and electrolytes and acid
base balance. (5tth ed.). Elsevier/Mosby. Missouri. International
Trauma Anesthesia and Critical Care Society (Spring 2003). Fluid
management in trauma. Retrieved on December 24, 2003 at: www.itaccs.com Kee,
V., R., (August 2003). Hemodynamic pharmacology of intravenous
Vasopressors. Retrieved on December 27, 2003 at: www.findarticles.com/cf_dls/m0NUC/4_23/107140384/print.jhtml Kolecki,
P., MD., (204). Hypovolemic Shock. Retrieved on January 15, 2005 at: www.emedicine.com/emerg/topic532.htm Plaza,
I., L., (April 1998). Transfusion medicine update: Massive blood
transfusion. Retrieved on December 25, 2003 at: www.itxm.org/TMU1998/tmu4-98.htm
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