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24. Which of the following is TRUE in a thromboelastogra-
CHAPTER 4
Hemostasis, Surgical Bleeding, and Transfusion
phy (TEG) tracing?
A. The r-value represents the clotting factor activity and
initial fibrin formation and is increased with factor
deficiency or severe hemodilution.
B. K time is prolonged with hypofibrinogenemia and
significant factor deficiency.
C. Decreased (alpha) or ∝ angle is treated with cryopre-
cipitate transfusion or fibrinogen administration.
D. All of the above.
Answer: D
Several parameters are generated from the TEG tracing. The
r-value (reaction time) represents the time between the start
of the assay and initial clot formation. This reflects clotting
factor activity and initial fibrin formation and is increased
with factor deficiency or severe hemodilution. The k-time
(clot kinetics) is the time needed to reach specified clot
strength and represents the interactions of clotting factors and
platelets. As such, the k-time is prolonged with hypofibrinogenemia and significant factor deficiency. Prolonged r-value
and k-time are commonly addressed with plasma transfusions. The alpha or angle (∝) is the slope of the tracing and
reflects clot acceleration. The angle reflects the interactions
of clotting factors and platelets. The slope is decreased with
hypofibrinogenemia and platelet dysfunction. Decreased
angles are treated with cryoprecipitate transfusion or fibrinogen administration. The maximal amplitude (mA) is the
greatest height of the tracing and represents clot strength. Its
height is reduced with dysfunction or deficiencies in platelets or fibrinogen. Decreased mA is addressed with platelet
transfusion and, in cases where the angle is also decreased,
with cryoprecipitate (or fibrinogen) as well. The G-value is a
parametric measure derived from the mA value and reflects
overall clot strength or firmness. An increased G-value is
associated with hypercoagulability, whereas a decrease is seen
with hypocoagulable states. Finally, the LY30 is the amount
of lysis occurring in the clot, and the value is the percentage
of amplitude reduction at 30 minutes after mA is achieved.
The LY30 represents clot stability and presence of increased
fibrinolysis. (Schwartz 11th ed., p. 124.)
CHAPTER 5
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Shock
1. Shock caused by a large tension pneumothorax is categorized as:
A. Traumatic shock.
B. Vasodilatory shock.
C. Cardiogenic shock.
D. Obstructive shock.
Answer: D
In 1934, Blalock proposed four categories of shock: hypovolemic, vasogenic, neurogenic, and cardiogenic. Hypovolemic
shock, the most common type, results from loss of circulating blood volume. This may result from loss of whole
blood (hemorrhagic shock), plasma, interstitial fluid (bowel
obstruction), or a combination. Vasogenic shock results from
decreased resistance within capacitance vessels, usually seen
in sepsis. Neurogenic shock is a form of vasogenic shock in
which spinal cord injury or spinal anesthesia causes vasodilation due to acute loss of sympathetic vascular tone. Cardio-
genic shock results from failure of the heart as a pump, as in
arrhythmias, or acute myocardial infarction (MI).
In recent clinical practice, further classification has described
six types of shock: hypovolemic, septic (vasodilatory), neurogenic, cardiogenic, obstructive, and traumatic shock. Obstruc-
tive shock is a form of cardiogenic shock that results from
mechanical impediment to circulation leading to depressed
cardiac output rather than primary cardiac failure. This
includes etiologies such as pulmonary embolism or tension
pneumothorax. In traumatic shock, soft tissue and bony injury
lead to the activation of inflammatory cells and the release of
circulating factors, such as cytokines and intracellular molecules that modulate the immune response. Recent investigations have revealed that the inflammatory mediators released
in response to tissue injury (damage-associated molecular
patterns [DAMPs]) are recognized by many of the same cellular receptors (pattern recognition receptors [PRRs]) and
activate similar signaling pathways as do bacterial products
elaborated in sepsis (pathogen-associated molecular patterns
[PAMPs]), such as lipopolysaccharide. These effects of tissue
injury are combined with the effects of hemorrhage, creating
a more complex and amplified deviation from homeostasis.
(See Schwartz 11th ed., p. 150.)
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2. What is TRUE about baroreceptors?
CHAPTER 5
A. Volume receptors can be activated in hemorrhage
with reduction in left atrial pressure.
B. Receptors in the aortic arch and carotid bodies inhibit
the autonomic nervous system when stretched.
C. When baroreceptors are stretched, they induced
increased autonomic nervous system output and pro-
Shock
duce constriction of peripheral vessels.
D. None of the above.
3. Chemoreceptors in the aorta and carotid bodies do NOT
sense which of the following?
A. Changes in O2 tension
B. H+ ion concentration
C. HCO
–
concentration
3
D. Carbon dioxide levels
Answer: B
Baroreceptors also are an important afferent pathway in initiation of adaptive responses to shock. Volume receptors, sensitive to changes in both chamber pressure and wall stretch, are
present within the atria of the heart. They become activated
with low-volume hemorrhage or mild reductions in right
atrial pressure. Receptors in the aortic arch and carotid bodies respond to alterations in pressure or stretch of the arterial
wall, responding to larger reductions in intravascular volume
or pressure. These receptors normally inhibit induction of
the autonomic nervous system. When activated, these baroreceptors diminish their output, thus disinhibiting the effect
of the autonomic nervous system. The autonomic nervous
system then increases its output, principally via sympathetic
activation at the vasomotor centers of the brain stem, producing centrally mediated constriction of peripheral vessels.
(See Schwartz 11th ed., p. 134.)
Answer: C
Chemoreceptors in the aorta and carotid bodies are sensitive to
changes in O2 tension, H+ ion concentration, and carbon dioxide (CO2) levels. Stimulation of the chemoreceptors results in
vasodilation of the coronary arteries, slowing of the heart rate,
and vasoconstriction of the splanchnic and skeletal circulation.
In addition, a variety of protein and nonprotein mediators
are produced at the site of injury as part of the inflammatory
response, and they act as afferent impulses to induce a host
response. These mediators include histamine, cytokines, eicosanoids, and endothelins. (See Schwartz 11th ed., p. 134.)
4. Neurogenic shock is characterized by the presence of:
A. Cool, moist skin.
B. Increased cardiac output.
C. Decreased peripheral vascular resistance.
D. Decreased blood volume.
5. When a patient with hemorrhagic shock is resuscitated
using an intravenous colloid solution rather than lactated Ringer’s solution, all of the following statements are
TRUE EXCEPT:
A. Circulating levels of immunoglobulins are decreased.
B. Colloid solutions may bind to the ionized fraction of
serum calcium.
C. Endogenous production of albumin is decreased.
D. Extracellular fluid volume deficit is restored.
Answer: C
Neurogenic shock is caused by loss of arteriolar and venular
tone in response to paralysis (such as occurs with high spinal anesthesia), acute gastric dilatation, or sudden pain or
unpleasant sights; as such, it is characterized by a decrease in
peripheral vascular resistance. Affected patients usually present with warm, dry skin, a pulse rate that is slower than normal, and hypotension. A normovolemic state usually exists,
and urine output is generally well maintained. Although
blood volume measurements indicate a normal intravascular
volume, because of the greatly increased reservoir capacity of
the arterioles and venules, there is a decrease in cardiac output
secondary to decreased venous return to the right side of the
heart. (See Schwartz 11th ed., p. 151.)
Answer: D
Because of higher osmotic pressure, colloid solutions draw
extracellular fluid into the vascular space, increasing the
extracellular fluid deficit. In addition, the ionized fraction
of serum calcium is decreased, circulating levels of immunoglobulin drop; and reaction to tetanus toxoid given to the
patient suffering from major trauma is decreased. Endogenous production of albumin also decreases. Colloid resuscitation is no more effective than crystalloid resuscitation, and
it is more expensive and its use in bleeding trauma patients
is associated with an increased risk of death. (See Schwartz
10th ed., p. 144.)
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6. In hemorrhage, larger arterioles vasoconstrict in response
to the sympathetic nervous system. Which categories of
shock are associated with vasodilation of larger arterioles?
A. Septic shock
B. Cardiogenic shock
C. Neurogenic shock
D. A and C
7. Which of the following is TRUE about anti-diuretic hormone (ADH) production in injured patients?
A. ADH acts as a potent mesenteric vasoconstrictor.
B. ADH levels fall to normal within 2–3 days of the ini-
tial insult.
C. ADH decreases hepatic gluconeogenesis.
D. ADH secretion is mediated by the renin-angiotensin
system.
Answer: D
The microvascular circulation plays an integral role in regulating cellular perfusion and is significantly influenced in
response to shock. The microvascular bed is innervated by
the sympathetic nervous system and has a profound effect on
the larger arterioles. Following hemorrhage, larger arterioles
vasoconstrict; however, in the setting of sepsis or neurogenic
shock, these vessels vasodilate. Additionally, a host of other
vasoactive proteins, including vasopressin, angiotensin II,
and endothelin-1, also lead to vasoconstriction to limit organ
perfusion to organs such as skin, skeletal muscle, kidneys,
and the gastrointestinal (GI) tract to preserve perfusion of
the myocardium and central nervous system (CNS). (See
Schwartz 11th ed., p. 136.)
Answer: A
The pituitary also releases vasopressin or ADH in response to
hypovolemia, changes in circulating blood volume sensed by
baroreceptors and left atrial stretch receptors, and increased
plasma osmolality detected by hypothalamic osmoreceptors. Epinephrine, angiotensin II, pain, and hyperglycemia
increase production of ADH. ADH levels remain elevated
for about 1 week after the initial insult, depending on the
severity and persistence of the hemodynamic abnormalities. ADH acts on the distal tubule and collecting duct of
the nephron to increase water permeability, decrease water
and sodium losses, and preserve intravascular volume. Also
known as arginine vasopressin, ADH acts as a potent mesenteric vasoconstrictor, shunting circulating blood away
from the splanchnic organs during hypovolemia. This may
contribute to intestinal ischemia and predispose to intestinal
mucosal barrier dysfunction in shock states. Vasopressin also
increases hepatic gluconeogenesis and increases hepatic glycolysis. (See Schwartz 11th ed., p. 135.)
CHAPTER 5
Shock
8. Which of following occurs as a result of epinephrine and
norepinephrine?
A. Hepatic glycogenolysis
B. Hypoglycemia
C. Insulin sensitivity
D. Lipogenesis
9. A patient has a blood pressure of 70/50 mm Hg and a
serum lactate level of 30 mg/100 mL (normal: 6 to 16).
Their cardiac output is 1.9 L/min, and his central venous
pressure is 2 cm H2O. The most likely diagnosis is:
A. Congestive heart failure.
B. Cardiac tamponade.
C. Hypovolemic shock.
D. Septic shock.
Answer: A
Epinephrine and norepinephrine have a profound impact
on cellular metabolism. Hepatic glycogenolysis, gluconeogenesis, ketogenesis, skeletal muscle protein breakdown, and
adipose tissue lipolysis are increased by catecholamines. Cortisol, glucagon, and anti-diuretic hormone (ADH) also contribute to the catabolism during shock. Epinephrine induces
further release of glucagon, while inhibiting the pancreatic
β-cell release of insulin. The result is a catabolic state with glucose mobilization, hyperglycemia, protein breakdown, negative nitrogen balance, lipolysis, and insulin resistance during
shock and injury. The relative underuse of glucose by peripheral tissues preserves it for the glucose-dependent organs, such
as the heart and brain. (See Schwartz 11th ed., p. 137.)
Answer: C
The findings given in the question are characteristic of
hypovolemic shock, which can be defined as inadequate tissue perfusion secondary to an extracellular fluid loss. The
high lactate level is a result of anaerobic metabolism due to
decreased blood flow to tissues. The hemodynamic measurements indicate both low blood flow and low venous return.
The total combination is most consistent with a diagnosis of
hypovolemic shock. Pulmonary embolus, congestive heart
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CHAPTER 5
Shock
10. Which of the following cytokines is elevated after shock
and trauma and plays an important role in the development of diffuse alveolar damage and acute respiratory
distress syndrome (ARDS)?
A. IL-10
B. TNF-α
C. IL-6
D. IL-1
11. How does activation of the complement cascade contribute to proinflammatory activation following injury and
shock?
A. Mediates organ dysfunction through increased vascu-
lar permeability, smooth muscle cell contraction, and
adherence of neutrophils to vascular endothelium.
B. Binds to specific chemokine receptors and transduce
chemotactic signals to leukocyte.
C. Depresses cytokine production and improves some
aspects of immune function.
D. Releases a number of substances that may induce
cell or tissue injury, such as reactive O2 species, lipidperoxidation products, proteolytic enzymes, and
vasoactive mediators.
failure, and cardiac tamponade are all associated with a high
central venous pressure. Septic shock, particularly in its early
phases, is usually hyperdynamic, and affected patients have
a greater-than-normal cardiac output. Complete hemodynamic monitoring is vital in hypovolemic shock so that
prompt diagnosis and rational therapy can be expeditiously
carried out. (See Schwartz 11th ed., p. 141.)
Answer: C
IL-6 is elevated in response to hemorrhagic shock and correlates with mortality in shock states. IL-6 contributes to
organ injury after hemorrhage shock, especially alveolar
damage and ARDS. IL-10 is considered an anti-inflammatory
cytokine that may have immunosuppressive properties. Its
production is increased after shock and trauma, and it has
been associated with depressed immune function clinically,
as well as an increased susceptibility to infection. TNF-α
may be induced by bacteria or endotoxin and leads to the
development of shock and hypoperfusion, most commonly
observed in septic shock. IL-1 has similar actions to TNF-α,
and is especially notable for its production of the febrile
response to injury through the activation of prostaglandins.
(See Schwartz 11th ed., p. 138.)
Answer: A
The complement cascade can be activated by injury, shock,
and severe infection, and contributes to host defense and
proinflammatory activation. In trauma patients, the degree
of complement activation is proportional to the magnitude of injury and may serve as a marker for severity of
injury. Activated complement factors C3a, C4a, and C5a are
potent mediators of increased vascular permeability, smooth
muscle cell contraction, histamine and arachidonic acid
by-product release, and adherence of neutrophils to vascular endothelium. Activated complement acts synergistically
with endotoxin to induce the release of TNF-α and IL-1.
The development of acute respiratory distress syndrome
(ARDS) and multiple organ dysfunction syndrome (MODS)
in trauma patients correlates with the intensity of complement activation. Complement and neutrophil activation may
correlate with mortality in multiply injured patients. (See
Schwartz 11th ed., p. 140.)
12. A 70-kg male patient presents emergency department
(ED) following a gunshot wound to the left lower quadrant wound to the abdomen. His blood pressure is 88/62
and his heart rate is 122. He is alert, but confused and
intermittently combative with first responders. What
percent of blood volume has he lost?
A. 5%
B. 15%
C. 35%
D. 55%
Answer: C
The clinical signs of shock may be evidenced by agitation,
cool clammy extremities, tachycardia, weak or absent peripheral pulses, and hypotension. Such apparent clinical shock
results from at least 25% to 30% loss of the blood volume.
However, substantial volumes of blood may be lost before
the classic clinical manifestations of shock are evident. Thus,
when a patient is significantly tachycardic or hypotensive,
this represents both significant blood loss and physiologic
decompensation. The clinical and physiologic response to
hemorrhage has been classified according to the magnitude
of volume loss. Loss of up to 15% of the circulating volume (700–750 mL for a 70-kg patient) may produce little in
terms of obvious symptoms, while loss of up to 30% of the
circulating volume (1.5 L) may result in mild tachycardia,
tachypnea, and anxiety. Hypotension, marked tachycardia
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13. Vaso dilatory shock:
A. Is characterized by failure of vascular smooth muscle
to constrict due low levels of catecholamines.
B. Leads to suppression of the renin-angiotensin system.
C. Can also be caused by carbon monoxide poisoning.
D. Is similar to early cardiogenic shock.
(ie, pulse >110–120 beats per minute [bpm]), and confusion
may not be evident until >30% of the blood volume has been
lost; loss of 40% of circulating volume (2 L) is immediately
life-threatening, and generally requires operative control of
bleeding. (See Schwartz 11th ed., p. 141.)
Answer: C
In the peripheral circulation, profound vasoconstriction
is the typical physiologic response to the decreased arterial
pressure and tissue perfusion with hemorrhage, hypovolemia,
or acute heart failure. This is not the characteristic response
in vasodilatory shock. Vasodilatory shock is the result of dysfunction of the endothelium and vasculature secondary to
circulating inflammatory mediators and cells or as a response
to prolonged and severe hypoperfusion. Thus, in vasodilatory shock, hypotension results from failure of the vascular
smooth muscle to constrict appropriately. Vasodilatory shock
is characterized by peripheral vasodilation with resultant
hypotension and resistance to treatment with vasopressors.
Despite the hypotension, plasma catecholamine levels are
elevated, and the renin-angiotensin system is activated in
vasodilatory shock. The most frequently encountered form of
vasodilatory shock is septic shock. Other causes of vasodilatory shock include hypoxic lactic acidosis, carbon monoxide poisoning, decompensated and irreversible hemorrhagic
shock, terminal cardiogenic shock, and postcardiotomy
shock. Thus, vasodilatory shock seems to represent the final
common pathway for profound and prolonged shock of any
etiology. (See Schwartz 11th ed., p. 145.)
CHAPTER 5
Shock
14. A patient in septic shock remains hypotensive despite
adequate fluid resuscitation and initiation of norepinephrine. What is often given to patients with hypotension refractory to norepinephrine?
A. Dopamine
B. Arginine vasopressin
C. Dobutamine
D. Milrinone
15. Which of the following best describes the physiologic
response and best treatment for critically ill and septic
patients?
A. Hypoglycemia and increased insulin sensitivity best
treated with liberal maintenance of blood glucose
<215 mg/dL to reduce hypoglycemic-related neurologic derailments
B. Hyperglycemia and insulin resistance best treated
with liberal maintenance of blood glucose <215 mg/dL
to minimize mortality and septicemia
C. Hyperglycemia and insulin resistance best treated
with intensive maintenance of blood glucose between
80 and 110 mg/dL to reduce mortality and septicemia
D. Hypoglycemia and insulin resistance best treated
with intensive maintenance of blood glucose between
80 and 110 mg/dL to reduce hypoglycemic neurologic derailments, mortality, and septicemia
Answer: B
After first-line therapy of the septic patient with the rapid
administration of antibiotics, IV fluids, and intubation if necessary, vasopressors may be necessary to treat patients with
septic shock. Catecholamines are the vasopressors used most
often, with norepinephrine being the first-line agent followed
by epinephrine. Occasionally, patients with septic shock will
develop arterial resistance to catecholamines. Arginine vasopressin, a potent vasoconstrictor, is often efficacious in this
setting and is often added to norepinephrine. (See Schwartz
11th ed., p. 147.)
Answer: C
Hyperglycemia and insulin resistance are typical in critically
ill and septic patients, including patients without underlying diabetes mellitus. A recent study reported significant
positive impact of tight glucose management on outcome in
critically ill patients. The two treatment groups in this randomized, prospective study were assigned to receive intensive insulin therapy (maintenance of blood glucose between
80 and 110 mg/dL) or conventional treatment (infusion of
insulin only if the blood glucose level exceeded 215 mg/dL,
with a goal between 180 and 200 mg/dL). The mean morning glucose level was significantly higher in the conventional
treatment as compared to the intensive insulin therapy group
(153 vs 103 mg/dL). Mortality in the intensive insulin treatment group (4.6%) was significantly lower than in the conventional treatment group (8%), representing a 42% reduction in
mortality. This reduction in mortality was most notable in the
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CHAPTER 5
16. Cardiogenic shock:
Shock
A. Is most commonly an acute exacerbation of chronic
congestive heart failure.
B. Is secondary to inadequate intravascular volume.
C. Confers a mortality rate of 50%–80%.
D. Permissive hypotension reduces afterload resulting
in improved cardiac perfusion.
patients requiring longer than 5 days in the ICU. Furthermore,
intensive insulin therapy reduced episodes of septicemia by
46%, reduced duration of antibiotic therapy, and decreased
the need for prolonged ventilatory support and renal replacement therapy. (See Schwartz 11th ed., p. 147.)
Answer: C
Cardiogenic shock is defined clinically as circulatory pump
failure leading to diminished forward flow and subsequent
tissue hypoxia, in the setting of adequate intravascular volume. Hemodynamic criteria include sustained hypotension
(ie, SBP < 90 mmHg for at least 30 minutes), reduced cardiac
index (<2.2 L/min per square meter), and elevated pulmonary artery wedge pressure (>15 mm Hg). Mortality rates for
cardiogenic shock are 50% to 80%. Acute, extensive MI is the
most common cause of cardiogenic shock; a smaller infarction in a patient with existing left ventricular dysfunction
also may precipitate shock. Cardiogenic shock complicates
5% to 10% of acute myocardial infarction (MIs). Conversely,
cardiogenic shock is the most common cause of death in
patients hospitalized with acute MI. Although shock may
develop early after MI, it typically is not found on admission.
Seventy-five percent of patients who have cardiogenic shock
complicating acute MIs develop signs of cardiogenic shock
within 24 hours after onset of infarction (average 7 hours).
(See Schwartz 11th ed., p. 148.)
17. Treatment for cardiogenic shock includes:
A. Established circulatory support prior to addressing
associated respiratory failure.
B. Adequate oxygenation to ensure adequate myocar-
dial O2 delivery and liberal fluid administration to
improve peripheral perfusion.
C. Dopamine administration to increase cardiac out-
put and vasodilate peripheral vascular beds to total
peripheral resistance.
D. Intra-aortic balloon pump, initiated prior to cardio-
tonic medications.
Answer: C
After ensuring that an adequate airway is present and ventilation is sufficient, attention should be focused on support of
the circulation. Intubation and mechanical ventilation often
are required, if only to decrease work of breathing and facilitate sedation of the patient. Rapidly excluding hypovolemia
and establishing the presence of cardiac dysfunction are
essential. Treatment of cardiac dysfunction includes maintenance of adequate oxygenation to ensure adequate myocardial O2 delivery and judicious fluid administration to avoid
fluid overload and development of cardiogenic pulmonary
edema. When profound cardiac dysfunction exists, inotropic
support may be indicated to improve cardiac contractility
and cardiac output. Dobutamine primarily stimulates cardiac
β1-receptors to increase cardiac output, but may also vasodilate peripheral vascular beds, lower total peripheral resistance, and lower systemic blood pressure through effects on
β2-receptors. Ensuring adequate preload and intravascular
volume is therefore essential prior to instituting therapy with
dobutamine. Dopamine stimulates receptors (vasoconstriction), β1-receptors (cardiac stimulation), and β2-receptors
(vasodilation), with its effects on β-receptors predominating
at lower doses. Dopamine may be preferable to dobutamine
in treatment of cardiac dysfunction in hypotensive patients.
Patients whose cardiac dysfunction is refractory to cardiotonics may require mechanical circulatory support with an
intra-aortic balloon pump. Intra-aortic balloon pumping
increases cardiac output and improves coronary blood flow
by reduction of systolic afterload and augmentation of diastolic perfusion pressure. (See Schwartz 11th ed., p. 149.)
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18. Following a high-speed motor vehicle accident resulting
in multiple right-sided rib fractures and associated sternal fracture, your patient becomes increasingly hypotensive in route to the emergency department with no
response to 2 L of fluid administration. What signs and
symptoms indicate obstructive shock from a right-sided
tension pneumothorax?
A. Hypotension, tachycardia, jugular venous distension,
leftward tracheal deviation
B. Hypotension, tachycardia, jugular venous distension,
muffled heart sounds
C. Hypotension, tachycardia, rightward tracheal devia-
tion, absent right sided breath sounds
D. Hypotension, tachycardia, pulsus paradoxus
19. A 17-year-old woman dives off of a cliff into a shallow
river. Upon arrival to the emergency department, she is
alert and upset, hypotensive, bradycardic, and her cool
extremities do not withdraw to stimuli. What is the most
likely cause of his hypotension?
A. Inadequate circulatory blood volume
B. Lack of venous return of blood to the heart
C. Loss of vasoconstrictor impulses results in increased
vascular capacitance, decreased venous return, and
decreased cardiac output
D. Systemic release of endotoxin secondary to exposure
to and inoculation of pathogens
Answer: A
The diagnosis of tension pneumothorax should be made on
clinical examination. The classic findings include respiratory distress (in an awake patient), hypotension, diminished
breath sounds over one hemithorax, hyperresonance to percussion, jugular venous distention, and shift of mediastinal
structures to the unaffected side with tracheal deviation.
Cardiac tamponade also may be associated with dyspnea,
orthopnea, cough, peripheral edema, chest pain, tachycardia,
muffled heart tones, jugular venous distention, and elevated
central venous pressure. Beck’s triad consists of hypotension,
muffled heart tones, and neck vein distention. (See Schwartz
11th ed., p. 150.)
Answer: C
Neurogenic shock refers to diminished tissue perfusion as a
result of loss of vasomotor tone to peripheral arterial beds.
Loss of vasoconstrictor impulses results in increased vascular
capacitance, decreased venous return, and decreased cardiac
output. Neurogenic shock is usually secondary to spinal cord
injuries from vertebral body fractures of the cervical or high
thoracic region that disrupt sympathetic regulation of peripheral vascular tone. (See Schwartz 11th ed., p. 151.)
CHAPTER 5
Shock
20. What defines adequate resuscitation in the setting of
shock?
A. Resolution of hypotension and tachycardia with
decreased mixed venous
B. O2 debt is repaid, tissue acidosis is corrected, and
aerobic metabolism restored
C. Normalization of blood pressure in the emergency
department with blood products in a patient with
a positive focused assessment with sonography for
trauma examination
D. Resolution of hypotension and tachycardia without
pharmacologic intervention, but rising lactate
Answer: B
Recognition by care providers of the patient who is in the
compensated phase of shock is equally important, but more
difficult based on clinical criteria. Compensated shock exists
when inadequate tissue perfusion persists despite normalization of blood pressure and heart rate. Even with normalization of blood pressure, heart rate, and urine output, 80% to
85% of trauma patients have inadequate tissue perfusion, as
evidenced by increased lactate or decreased mixed venous O2
saturation. Persistent, occult hypoperfusion is frequent in the
ICU, with a resultant significant increase in infection rate and
mortality in major trauma patients. Patients failing to reverse
their lactic acidosis within 12 hours of admission (acidosis
that was persistent despite normal heart rate, blood pressure,
and urine output) developed an infection three times as often
as those who normalized their lactate levels within 12 hours
of admission. In addition, mortality was fourfold higher in
patients who developed infections. Both injury severity score
and occult hypotension (lactic acidosis) longer than 12 hours
were independent predictors of infection. Thus, recognition
of subclinical hypoperfusion requires information beyond
vital signs and urinary output.
Endpoints in resuscitation can be divided into systemic
or global parameters, tissue-specific parameters, and cellular
parameters. Global endpoints include vital signs, cardiac output,
pulmonary artery wedge pressure, O2 delivery and consumption, lactate, and base deficit. (See Schwartz 11th ed., p. 152.)
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21. Base deficit:
CHAPTER 5
A. Quantifies the magnitude of perfusion deficit.
B. Is representative of perfusion status, but not the risk
C. Which is persistently elevated is evidence of hospital-
D. Does not provide additional information in clinical
Shock
of death.
acquired infection following a traumatic event.
resuscitation when serum lactates can be assessed.
Answer: A
Base deficit is the amount of base in millimoles that is
required to titrate 1 L of whole blood to a pH of 7.40 with
the sample fully saturated with O2 at 37°C (98.6°F) and a partial pressure of CO2 of 40 mm Hg. It usually is measured by
arterial blood gas analysis in clinical practice as it is readily
and quickly available. The mortality of trauma patients can
be stratified according to the magnitude of base deficit measured in the first 24 hours after admission. In a retrospective study of over 3000 trauma admissions, patients with a
base deficit worse than 15 mmol/L had a mortality of 70%.
Base deficit can be stratified into mild (3–5 mmol/L), moderate (6–14 mmol/L), and severe (15 mmol/L) categories, with
a trend toward higher mortality with worsening base deficit
in patients with trauma. Both the magnitude of the perfusion
deficit as indicated by the base deficit and the time required
to correct it are major factors determining outcome in shock.
Indeed, when elevated base deficit persists (or lactic
acidosis) in the trauma patient, ongoing bleeding is often
the etiology. Trauma patients admitted with a base deficit
>15 mmol/L required twice the volume of fluid infusion and
six times more blood transfusion in the first 24 hours compared to patients with mild acidosis. Transfusion requirements increased as base deficit worsened and ICU and
hospital lengths of stay increased. Mortality increased as base
deficit worsened; the frequency of organ failure increased
with greater base deficit. The probability of trauma patients
developing acute respiratory distress syndrome (ARDS)
has been reported to correlate with severity of admission
base deficit and lowest base deficit within the first 24 hours
post injury. Persistently high base deficit is associated with
abnormal O2 utilization and higher mortality. Monitoring
base deficit in the resuscitation of trauma patients assists in
assessment of O2 transport and efficacy of resuscitation. (See
Schwartz 11th ed., p. 152.)
CHAPTER 6
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Surgical Infection
1. Macrophage response to microbes includes:
A. Genome-encoded pattern recognition receptors to
invading microbes (pathogen-associated molecular
patterns [PAMPs] and danger-associated molecular
patterns [DAMPs]).
B. Upregulation of cytokine synthesis.
C. Secretion of cytokines.
D. All of the Above.
2. Which of the following is NOT a component of systemic
inflammatory response syndrome (SIRS)?
A. Temperature
B. WBC count
C. Blood pressure
D. Heart rate
Answer: D
The response in macrophages is initiated by genomeencoded pattern recognition receptors that respond to
invading microbes. With exposure to a foreign organism,
these receptors recognize microbial PAMPs and endogenous DAMPs. Toll-like receptors (TLRs) are a well-defined
example of a PAMP that plays an important role in pathogen
signaling. Resident macrophages secrete a wide array of substances in response to the aforementioned processes, some
of which appear to regulate the cellular components of the
host defense response. This results in recruitment and proliferation of inflammatory cells. Macrophage cytokine synthesis is upregulated. Secretion of tumor necrosis factor-alpha
(TNF-α); interleukins (IL)-1β, 6, and 8; and gamma interferon (IFN-γ) occurs within the tissue milieu and depends
on the magnitude of the host defense response, the systemic
circulation. Concurrently, a counterregulatory response is
initiated consisting of binding protein (TNF-BP), cytokine
receptor antagonists (eg, IL-1ra), and anti-inflammatory
cytokines (IL-4 and IL-10). (Schwartz 11th ed., p. 160.)
Answer: C
Infection is defined by the presence of microorganisms in host
tissue or the bloodstream. The classic findings of rubor, calor,
and dolor in areas such as the skin or subcutaneous tissue are
common at the site of infection. Most infections in normal
individuals with intact host defenses are associated with these
local manifestations, plus systemic manifestations such as
elevated temperature, elevated white blood cell (WBC) count,
tachycardia, or tachypnea. The systemic manifestations noted
previously comprise what has been termed the systemic
inflammatory response syndrome (SIRS). SIRS reflects a proinflammatory state in response to a variety of disease processes,
including infection, pancreatitis, polytrauma, malignancy,
and burns. There are a variety of systemic manifestations of
infection, with the classic factors of fever, tachycardia, and
tachypnea broadened to include a variety of other variables
(Schwartz 11th ed., p. 160.)
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