Critical Care and Clinical Skills

Question 1

What is the half-life of phenobarbital?
A. 6 hours
B. 12 hours
C. 24 hours
D. 100 hours
E. 140 hours

Answer 1

A. 6 hours
B. 12 hours
C. 24 hours
**D. 100 hours **
E. 140 hours

The half-life of phenobarbital is generally between 98
and 120 hours in the average adult. Phenobarbital is largely
metabolized by the liver, although 20 to 30% of the drug can
be excreted unchanged in the urine. Barbiturates bind the
GABAA receptor in the CNS, which facilitates Cl-mediated
inhibitory postsynaptic potentials. Phenobarbital is often
used in the treatment of partial and generalized tonic-clonic
seizures in neonates (Katzung, pp. 37, 358-359, 393-394)

Question 2

What is the initial treatment of choice in a patient with
symptomatic hyperkalemia associated with ECG changes?
A. Furosemide
B. Insulin/glucose
C. Bicarbonate
D. I(ayexalate
E. Calcium gluconate

Answer 2

A. Furosemide
B. Insulin/glucose
C. Bicarbonate
D. I(ayexalate
E. Calcium gluconate

Calcium gluconate is the initial treatment of choice for
symptomatic hyperkalemia because it rapidly antagonizes
the effects of hyperkalemia directly at the plasma membrane
level. The effects of calcium gluconate are short-lived,
however, and other therapies should be instituted simultaneously. Loop diuretics (furosemide) can increase renal
potassium excretion, I<ayexalate enhances gastrointestinal
potassium excretion, and bicarbonate and insulin/glucose
induce intracellular shifts of potassium primarily into
muscle cells. Sodium bicarbonate is less effective in patients
with renal failure, however, and can actually bind calcium;
therefore its utility is limited. The definitive treatment for
patients with chronic hyperkalemia is hemodialysis (Marino,
pp. 655- 658).

Question 3

What is the treatment of choice for paroxysmal supraventricular tachycardia (SVT)?
A. Electric cardioversion
B. Adenosine
C. Calcium antagonists
D. 0 blockers
E. Digoxin

Answer 3

A. Electric cardioversion
**B. Adenosine **
C. Calcium antagonists
D. 0 blockers
E. Digoxin

Paroxysmal supraventricular tachycardia (AV-nodal
re-entrant tachycardi a) results from re-entry of impulses
from an ectopic source. Adenosine blocks the positive
inotropic effects of catecholamines, slows conduction at
the AV node, and dilates coronary arteries. Additionally,
the effects of adenosine are short-lived, so it does not elicit
significant myocardial depression. It is these characteristics
of adenosine that make it the drug of choice in the treatment
of paroxysmal SVT over calcium antagonists (Marino,
pp. 329- 330).

Question 4

Which of the following disorders is most commonly
associated with prominent leukocyte casts on microscopic
urinalysis?
A. Acute interstitial nephritis
B. Acute tubular necrosis
C. Minimal change disease
D. Cryoglobulinemia
E. None of the above

Answer 4

A. Acute interstitial nephritis
B. Acute tubular necrosis
C. Minimal change disease
D. Cryoglobulinemia
E. None of the above

Acute interstitial nephritis (AI.t\f) is a common cause of
acute renal failure and is usually associated with infections
or hypersensitivity drug reactions. AlN is characterized by a
decrease in the glomerular filtration rate, often with oliguria .
Urinalysis often exhibits hematuria, mild proteinuria, an
elevated fractional excretion of sodium, eosinophilia, and
leukocyte casts with AIN. Acute tubular necrosis (A TN)
most commonly results from renal hypoperfusion and
is characterized by acute renal failure, an elevated fractional excretion of sodium, and granular casts on urinalysis.
Cryoglobulinemia can result in acute renal insufficiency secondary to the deposition of immunoglobulins in the renal
parenchyma and is usually associated with the nephrotic
syndrome. Minimal change disease is associated with proteinuria and the nephrotic syndrome as well (Cecil, pp. 579,
581-583; Marino, pp. 621- 622, 626).

Question 5

Match the following clinical characteristics with
the corresponding electrolyte abnormality, using each answer
once, more than once, or not at all:

Muscle weakness, altered mental status, U waves on ECG
A. Hyponatremia
B. Hypocalcemia
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Answer 5

A. Hyponatremia
B. Hypocalcemia
C. Hypomagnesemia
**D. Hypokalemia **
E. Hypophosphatemia
F. Hypochloremia

Symptomatic hyponatremia (usually
120 mEq/L or less) can result in generalized seizures,
metabolic encephalopathy, depressed level of consciousness,
acute respiratory distress syndrome, muscle weakness, and
even cerebral edema and elevated intracranial pressure.
Hypokalemia can result in muscle wealmess, altered mental
status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval); however, isolated hypokalemia
does not result in significant cardiac arrhythmias. Hypomagnesemia is very common in the lCU setting and is often
associated with depletion of other electrolytes (phosphate,
calcium, potassium). Symptomatic hypomagnesemia has
been associated with digitalis cardiotoxicity, torsades de
pointes, tremors, hyperreflexia, and generalized seizures.
Hypocalcemia can result in decreased cardiac output,
hypotension, ventricular ectopy, hyperreflexia , generalized
seizures, and tetany. Mild to moderate hypophosphatemia
is often asymptomatic, while severe phosphate depletion
can be associated with decreased cardiac output, hemolytic
anemia, impaired tissue oxygen availability, and muscle
weakness (Marino, pp. 643-644, 650- 651, 662-665, 677,
683- 685).

Question 6

Match the following clinical characteristics with
the corresponding electrolyte abnormality, using each answer
once, more than once, or not at all:

Associated with other electrolyte abnormalities and
torsades de pointes
A. Hyponatremia
B. Hypocalcemia
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Answer 6

A. Hyponatremia
B. Hypocalcemia
**C. Hypomagnesemia **
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Symptomatic hyponatremia (usually
120 mEq/L or less) can result in generalized seizures,
metabolic encephalopathy, depressed level of consciousness,
acute respiratory distress syndrome, muscle weakness, and
even cerebral edema and elevated intracranial pressure.
Hypokalemia can result in muscle wealmess, altered mental
status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval); however, isolated hypokalemia
does not result in significant cardiac arrhythmias. Hypomagnesemia is very common in the lCU setting and is often
associated with depletion of other electrolytes (phosphate,
calcium, potassium). Symptomatic hypomagnesemia has
been associated with digitalis cardiotoxicity, torsades de
pointes, tremors, hyperreflexia, and generalized seizures.
Hypocalcemia can result in decreased cardiac output,
hypotension, ventricular ectopy, hyperreflexia , generalized
seizures, and tetany. Mild to moderate hypophosphatemia
is often asymptomatic, while severe phosphate depletion
can be associated with decreased cardiac output, hemolytic
anemia, impaired tissue oxygen availability, and muscle
weakness (Marino, pp. 643-644, 650- 651, 662-665, 677,
683- 685).

Question 7

Match the following clinical characteristics with
the corresponding electrolyte abnormality, using each answer
once, more than once, or not at all:

Muscle weakness, decreased cardiac output, hemolytic
anemia
A. Hyponatremia
B. Hypocalcemia
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Answer 7

A. Hyponatremia
B. Hypocalcemia
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Symptomatic hyponatremia (usually
120 mEq/L or less) can result in generalized seizures,
metabolic encephalopathy, depressed level of consciousness,
acute respiratory distress syndrome, muscle weakness, and
even cerebral edema and elevated intracranial pressure.
Hypokalemia can result in muscle wealmess, altered mental
status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval); however, isolated hypokalemia
does not result in significant cardiac arrhythmias. Hypomagnesemia is very common in the lCU setting and is often
associated with depletion of other electrolytes (phosphate,
calcium, potassium). Symptomatic hypomagnesemia has
been associated with digitalis cardiotoxicity, torsades de
pointes, tremors, hyperreflexia, and generalized seizures.
Hypocalcemia can result in decreased cardiac output,
hypotension, ventricular ectopy, hyperreflexia , generalized
seizures, and tetany. Mild to moderate hypophosphatemia
is often asymptomatic, while severe phosphate depletion
can be associated with decreased cardiac output, hemolytic
anemia, impaired tissue oxygen availability, and muscle
weakness (Marino, pp. 643-644, 650- 651, 662-665, 677,
683- 685).

Question 8

Match the following clinical characteristics with
the corresponding electrolyte abnormality, using each answer
once, more than once, or not at all:

Decreased cardiac output, hyperreflexia , tetany
A. Hyponatremia
B. Hypocalcemia
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Answer 8

A. Hyponatremia
**B. Hypocalcemia **
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Symptomatic hyponatremia (usually
120 mEq/L or less) can result in generalized seizures,
metabolic encephalopathy, depressed level of consciousness,
acute respiratory distress syndrome, muscle weakness, and
even cerebral edema and elevated intracranial pressure.
Hypokalemia can result in muscle wealmess, altered mental
status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval); however, isolated hypokalemia
does not result in significant cardiac arrhythmias. Hypomagnesemia is very common in the lCU setting and is often
associated with depletion of other electrolytes (phosphate,
calcium, potassium). Symptomatic hypomagnesemia has
been associated with digitalis cardiotoxicity, torsades de
pointes, tremors, hyperreflexia, and generalized seizures.
Hypocalcemia can result in decreased cardiac output,
hypotension, ventricular ectopy, hyperreflexia , generalized
seizures, and tetany. Mild to moderate hypophosphatemia
is often asymptomatic, while severe phosphate depletion
can be associated with decreased cardiac output, hemolytic
anemia, impaired tissue oxygen availability, and muscle
weakness (Marino, pp. 643-644, 650- 651, 662-665, 677,
683- 685).

Question 9

Match the following clinical characteristics with
the corresponding electrolyte abnormality, using each answer
once, more than once, or not at all:

Encephalopathy, cerebral edema, and seizures
A. Hyponatremia
B. Hypocalcemia
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Answer 9

**A. Hyponatremia **
B. Hypocalcemia
C. Hypomagnesemia
D. Hypokalemia
E. Hypophosphatemia
F. Hypochloremia

Symptomatic hyponatremia (usually
120 mEq/L or less) can result in generalized seizures,
metabolic encephalopathy, depressed level of consciousness,
acute respiratory distress syndrome, muscle weakness, and
even cerebral edema and elevated intracranial pressure.
Hypokalemia can result in muscle wealmess, altered mental
status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval); however, isolated hypokalemia
does not result in significant cardiac arrhythmias. Hypomagnesemia is very common in the lCU setting and is often
associated with depletion of other electrolytes (phosphate,
calcium, potassium). Symptomatic hypomagnesemia has
been associated with digitalis cardiotoxicity, torsades de
pointes, tremors, hyperreflexia, and generalized seizures.
Hypocalcemia can result in decreased cardiac output,
hypotension, ventricular ectopy, hyperreflexia , generalized
seizures, and tetany. Mild to moderate hypophosphatemia
is often asymptomatic, while severe phosphate depletion
can be associated with decreased cardiac output, hemolytic
anemia, impaired tissue oxygen availability, and muscle
weakness (Marino, pp. 643-644, 650- 651, 662-665, 677,
683- 685).

Question 10

Match the most effective anticonvulsant with the
corresponding seizure disorder. Answers may be used once,
more than once, or not at all:

Ethosuximide
A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Answer 10

**A. Absence **
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Isolated absence seizures
(petit mal epilepsy) are generally treated with ethosuximide;
however, valproic acid is the agent of choice if the patient
also experiences generalized tonic-clonic seizures. LennoxGastaut syndrome is a heterogenous disorder characterized
by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 Hz on EEG. Valproic acid is the
initial treatment of choice for this disorder; however, less
than 10% of all patients with Lennox-Gastaut syndrome
achieve effective seizure control with Single-agent anticonvulsant therapy. Infantile spasms (West syndrome) occur in
children less than 6 1110nths of age and are associated with
tuberous sclerosis, cerebral malformations, and metabolic
disorders. The treatment of choice for infantile spasms is
ACTH. Several anticonvulsants are utilized in the treatment
of generalized tonic-clonic seizures; however, phenytoin is
the traditional first-line agent. Phenobarbital is the drug of
choice in the treatment of neonatal seizures, but phenytoin
and lorazepam are often added with inadequate seizure
control. Carbamazepine is the agent of choice in the treatment of compl ex partial seizures and is particularly effective
in preventing secondary generalization (Merritt, pp. 813-
826).

Question 11

Match the most effective anticonvulsant with the
corresponding seizure disorder. Answers may be used once,
more than once, or not at all:

Valproic acid
A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Answer 11

A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
**F. Lennox-Gastaut syndrome **
G. None of the above

Isolated absence seizures
(petit mal epilepsy) are generally treated with ethosuximide;
however, valproic acid is the agent of choice if the patient
also experiences generalized tonic-clonic seizures. LennoxGastaut syndrome is a heterogenous disorder characterized
by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 Hz on EEG. Valproic acid is the
initial treatment of choice for this disorder; however, less
than 10% of all patients with Lennox-Gastaut syndrome
achieve effective seizure control with Single-agent anticonvulsant therapy. Infantile spasms (West syndrome) occur in
children less than 6 1110nths of age and are associated with
tuberous sclerosis, cerebral malformations, and metabolic
disorders. The treatment of choice for infantile spasms is
ACTH. Several anticonvulsants are utilized in the treatment
of generalized tonic-clonic seizures; however, phenytoin is
the traditional first-line agent. Phenobarbital is the drug of
choice in the treatment of neonatal seizures, but phenytoin
and lorazepam are often added with inadequate seizure
control. Carbamazepine is the agent of choice in the treatment of compl ex partial seizures and is particularly effective
in preventing secondary generalization (Merritt, pp. 813-
826).

Question 12

Match the most effective anticonvulsant with the
corresponding seizure disorder. Answers may be used once,
more than once, or not at all:

ACTH
A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Answer 12

A. Absence
**B. Infantile spasms **
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Isolated absence seizures
(petit mal epilepsy) are generally treated with ethosuximide;
however, valproic acid is the agent of choice if the patient
also experiences generalized tonic-clonic seizures. LennoxGastaut syndrome is a heterogenous disorder characterized
by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 Hz on EEG. Valproic acid is the
initial treatment of choice for this disorder; however, less
than 10% of all patients with Lennox-Gastaut syndrome
achieve effective seizure control with Single-agent anticonvulsant therapy. Infantile spasms (West syndrome) occur in
children less than 6 1110nths of age and are associated with
tuberous sclerosis, cerebral malformations, and metabolic
disorders. The treatment of choice for infantile spasms is
ACTH. Several anticonvulsants are utilized in the treatment
of generalized tonic-clonic seizures; however, phenytoin is
the traditional first-line agent. Phenobarbital is the drug of
choice in the treatment of neonatal seizures, but phenytoin
and lorazepam are often added with inadequate seizure
control. Carbamazepine is the agent of choice in the treatment of compl ex partial seizures and is particularly effective
in preventing secondary generalization (Merritt, pp. 813-
826).

Question 13

Match the most effective anticonvulsant with the
corresponding seizure disorder. Answers may be used once,
more than once, or not at all:

Phenytoin
A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Answer 13

A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
**E. Generalized tonic-clonic **
F. Lennox-Gastaut syndrome
G. None of the above

Isolated absence seizures
(petit mal epilepsy) are generally treated with ethosuximide;
however, valproic acid is the agent of choice if the patient
also experiences generalized tonic-clonic seizures. LennoxGastaut syndrome is a heterogenous disorder characterized
by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 Hz on EEG. Valproic acid is the
initial treatment of choice for this disorder; however, less
than 10% of all patients with Lennox-Gastaut syndrome
achieve effective seizure control with Single-agent anticonvulsant therapy. Infantile spasms (West syndrome) occur in
children less than 6 1110nths of age and are associated with
tuberous sclerosis, cerebral malformations, and metabolic
disorders. The treatment of choice for infantile spasms is
ACTH. Several anticonvulsants are utilized in the treatment
of generalized tonic-clonic seizures; however, phenytoin is
the traditional first-line agent. Phenobarbital is the drug of
choice in the treatment of neonatal seizures, but phenytoin
and lorazepam are often added with inadequate seizure
control. Carbamazepine is the agent of choice in the treatment of compl ex partial seizures and is particularly effective
in preventing secondary generalization (Merritt, pp. 813-
826).

Question 14

Match the most effective anticonvulsant with the
corresponding seizure disorder. Answers may be used once,
more than once, or not at all:

Phenobarbital
A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Answer 14

A. Absence
B. Infantile spasms
C. Complex partial
**D. Neonatal seizures **
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Isolated absence seizures
(petit mal epilepsy) are generally treated with ethosuximide;
however, valproic acid is the agent of choice if the patient
also experiences generalized tonic-clonic seizures. LennoxGastaut syndrome is a heterogenous disorder characterized
by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 Hz on EEG. Valproic acid is the
initial treatment of choice for this disorder; however, less
than 10% of all patients with Lennox-Gastaut syndrome
achieve effective seizure control with Single-agent anticonvulsant therapy. Infantile spasms (West syndrome) occur in
children less than 6 1110nths of age and are associated with
tuberous sclerosis, cerebral malformations, and metabolic
disorders. The treatment of choice for infantile spasms is
ACTH. Several anticonvulsants are utilized in the treatment
of generalized tonic-clonic seizures; however, phenytoin is
the traditional first-line agent. Phenobarbital is the drug of
choice in the treatment of neonatal seizures, but phenytoin
and lorazepam are often added with inadequate seizure
control. Carbamazepine is the agent of choice in the treatment of compl ex partial seizures and is particularly effective
in preventing secondary generalization (Merritt, pp. 813-
826).

Question 15

Match the most effective anticonvulsant with the
corresponding seizure disorder. Answers may be used once,
more than once, or not at all:

Carbamazepine
A. Absence
B. Infantile spasms
C. Complex partial
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Answer 15

A. Absence
B. Infantile spasms
**C. Complex partial **
D. Neonatal seizures
E. Generalized tonic-clonic
F. Lennox-Gastaut syndrome
G. None of the above

Isolated absence seizures
(petit mal epilepsy) are generally treated with ethosuximide;
however, valproic acid is the agent of choice if the patient
also experiences generalized tonic-clonic seizures. LennoxGastaut syndrome is a heterogenous disorder characterized
by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 Hz on EEG. Valproic acid is the
initial treatment of choice for this disorder; however, less
than 10% of all patients with Lennox-Gastaut syndrome
achieve effective seizure control with Single-agent anticonvulsant therapy. Infantile spasms (West syndrome) occur in
children less than 6 1110nths of age and are associated with
tuberous sclerosis, cerebral malformations, and metabolic
disorders. The treatment of choice for infantile spasms is
ACTH. Several anticonvulsants are utilized in the treatment
of generalized tonic-clonic seizures; however, phenytoin is
the traditional first-line agent. Phenobarbital is the drug of
choice in the treatment of neonatal seizures, but phenytoin
and lorazepam are often added with inadequate seizure
control. Carbamazepine is the agent of choice in the treatment of compl ex partial seizures and is particularly effective
in preventing secondary generalization (Merritt, pp. 813-
826).

Question 16

Which of the following characteristics is NOT applicable
to synchronized intermittent mandatory ventilation (SJi-IV)?
A. Delivers volume-cycled breaths
B. Often combined with pressure support to overcome
the resistance of the ventilator circuit tubing
C. Allows spontaneous breaths between ventilatordelivered breaths
D. Associated with a decreased work of breathing
E. Associated with impaired ventricular filling

Answer 16

A. Delivers volume-cycled breaths
B. Often combined with pressure support to overcome
the resistance of the ventilator circuit tubing
**C. Allows spontaneous breaths between ventilatordelivered breaths **
D. Associated with a decreased work of breathing
E. Associated with impaired ventricular filling

SlMV was developed secondary to complications (e.g. ,
hyperinflation and overventilation) that can arise in patients
on assist-control ventilation (ACV) with rapid respiratory
rates. SIMV delivers volume-cycled breaths at a preselected
rate that are synchronized to the patient’s spontaneous
breaths. Additionally, SL\·1V allows spontaneous breaths to
occur between ventilator-delivered breaths. Spontaneous
breaths during SL\fV occur through a high-resistance circuit
with a unidirectional valve , which results in an increased
work of breathing and potential for respiratory muscle
fatigue. The addition of pressure support facilitates spontaneous breaths and can limit increases in work of breathing
(and respiratory muscle fatigue) with SINN. Any form of
positive-pressure mechanical ventilation can be associated
with impaired ventricular filling and concomitant reductions
in cardiac output (Marino, pp. 434- 438).

Question 17

Which of the following characteristics is NOT associated
with extrinsic positive end-expiratory pressure (PEEP)?
A. Facilitates alveolar recruitment
B. Reduces pulmonary edema
C. Increases mean intrathoracic pressure
D. Decreases intrapulmonary shunt
E. Reduces cardiac output

Answer 17

A. Facilitates alveolar recruitment
**B. Reduces pulmonary edema **
C. Increases mean intrathoracic pressure
D. Decreases intrapulmonary shunt
E. Reduces cardiac output

Normally, the alveolar pressure at the end of expira -
tion is equal to atmospheric pressure. The addition of PEEP
(extrinsic PEEP) results in an elevated alveolar pressure at
the end of expiration by stopping exha lation when the preselected pressure is reached. PEEP results in increases in endexpiratory and mean intrathoracic pressures. PEEP tends
to prevent alveolar collapse and facilitate alveolar reopening (recruitment), which results in improved gas exchange
(decreased intrapulmonary shunt) and increased lung
compliance. The addition of PEEP can result in decreased
cardiac filling and cardiac output, especiaLly in hypovolemic
patients; this effect is independent of the absolute value of
the extrinsic PEEP. The increases in mean intrathoracic
pressure that are secondary to extrinsic PEEP are directly
related to the observed decreases in cardiac output. The
application of PEEP does not reduce pulmonary edema
and can, in fact, exacerbate pulmonary edema secondary to
alveolar overdistention and impaired pulmonary lymphatic
drainage (Marino, pp. 382-383, 441- 445).

Question 18

All of the following are associated with acute respiratory
distress syndrome (ARDS) EXCEPT?
A. Hypoxia
B. Diffuse pulmonary infiltrates
C. Hypercapnia
D. The addition of positive end-expiratory pressure (PEEP)
prevents alveolar collapse and allows for reduction of
the Fi02 to nontoxic levels
E. Often exhibits a PA02 /Fi02 ratio > 200 mmHg

Answer 18

A. Hypoxia
B. Diffuse pulmonary infiltrates
C. Hypercapnia
D. The addition of positive end-expiratory pressure (PEEP)
prevents alveolar collapse and allows for reduction of
the Fi02 to nontoxic levels
E. Often exhibits a PA02 /Fi02 ratio > 200 mmHg

ARDS is characterized by the acute onset of diffuse
pulmonary infiltrates and hypoxemia that is refractory to
elevations in Fi02 . Lung-protective ventilatory strategies
with ARDS include the utilization of lower tidal volumes (7 to
10 cc/l{g) than with other traditional forms of ventilation to
keep peak inspiratory pressures less than 3S cm H20. The
addition of PEEP with ARDS prevents alveolar collapse (with
the lower tidal volumes) and allows the reduction of the Fi02
to nontoxic levels « 60%). Patients with ARDS who exhibit
refractory hypoxemia or hypercapnia are often placed on
inverse-ratio ventilation (IRV) , which results in prolonged lung inflation times and concomitant alveolar recruitment
(Marino, pp. 381-383, 440).

Question 19

Which of the following characteristics is NOT associated
with auto-PEEP (intrinsic PEEP or hyperinflation) ?
A. Large inflation volumes
B. Lower respiratory rates
C. Inverse ratio ventilation
D. Asthma
E. Pneumothorax

Answer 19

A. Large inflation volumes
**B. Lower respiratory rates **
C. Inverse ratio ventilation
D. Asthma
E. Pneumothorax

Intrinsic PEEP (occult PEEP) results from incomplete
alveolar emptying during expiration. The development of
intrinsic PEEP is associated with large inflation volumes,
rapid respiratory rates, decreases in exhalation time (inverse
ratio ventilation), and airway obstruction (e.g., asthma and
COPD). High levels of intrinsic PEEP are associated with
decreased cardiac output, alveolar rupture (volutrauma)
with possible pneumothorax, increased work of breathing,
and elevations in plateau pressures (Marino, pp. 462-464).

Question 20

Which of the following ECG changes can be observed in
patients with pulmonary emboli?
1. Tachycardia
2. Nonspecific ST changes
3. Large Q wave in lead III
4. Inverted T wave in lead III

A. 1,2, and3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 20

A. 1,2, and3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

ECG changes in acute pulmonary emboli include sinus
tachycardia (most common), inverted T waves in leads VI to
V.l , right axis deviation, right bundle branch block, and atrial
arrhythmias. The classic findings of “SI’ (1, T/ refers to the
presence of a wide S complex in lead I, a large Q wave in lead
III, and an inverted T wave in lead III, although these findings
are not very sensitive in the diagnosis of acute pulmonary
embolism. ALI of these ECG changes are usually transient
findings that resolve once the pulmonary arterial pressure
has normalized after the acute ictus (Cecil, p. 424).

Question 21

Which of the following is the first-line agent of choice in
the treatment of multifocal atrial tachycardia ?
A. IV magnesium
B. Verapamil
C. Metoprolol
D. Lidocaine
E. Electric cardioversion

Answer 21

**A. IV magnesium **
B. Verapamil
C. Metoprolol
D. Lidocaine
E. Electric cardioversion

Multifocal atrial tachycardia (MAT) exhibits multiple
P-wave morphologies and variable PR intervals on ECG, with
an irregular ventricular rate. MAT is associated with chronic
lung disease and theophylline, and has been associated
with hypokalemia, acute myocardial infarction, pulmonary
embolism, and congestive heart failure. ivlAT should initially
be treated with IV magneSium; theophylline should be
discontinued and any underlying hypokalemia corrected.
If these therapies are ineffective, verapamil or metoprolol
should be administered (Marino, pp. 328-329).

Question 22

Which of the following characteristics is associated with
cardiac tamponade ?
1. Jugular venous distention
2. Hypotension
3. Muffled heart sounds
4. A rise in the systolic blood pressure (> 10 mmI-Ig) with
inspiration onset

A. 1, 2, and3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 22

**A. 1, 2, and3 are correct **
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Cardiac tamponade is associated with Beck’s triad
(jugular venous distention, muffled heart sounds, hypotension) and pulsus paradoxus (d rop in systolic blood pressure
of at least 10 mm I-Ig with the onset of inspiration). Diastolic
pressures (CVP, PCWP, pulmonary artery diastolic pressure)
are often equalized with cardiac tamponade, and the diagnosiS
is often confirmed with transesophageal echocardiography.
The treatment of cardiac tamponade entails emergent
pericardiocentesis (Ma rino, pp. 255-256).

Question 23

A 48-year-old female with three children experiences the
acute onset of a fever three hours after receiving a blood
transfusion. What precautions should be taken prior to the
administration of a second transfusion?
A. Administer washed red cells
B. Administer leukocyte-poor red cells
C. Pretreatment with Tylenol
D. Investigate for the presence of IgA defiCiency
E. None of the above

Answer 23

A. Administer washed red cells
B. Administer leukocyte-poor red cells
**C. Pretreatment with Tylenol **
D. Investigate for the presence of IgA defiCiency
E. None of the above

Febrile nonhemolytic reactions are extremely common and accompany approximately 1% of all transfusions.
These reactions are secondary to antibodies in the recipient
blood that react to donor leukocytes and are more common
in multiparous women and a history of prior transfusions.
The fever usually occurs between 1 and 6 hours after the
transfusion and is not associated with other symptoms. The
ma.iority of patients who experience a febrile nonhemolytic
reaction will not experience a second fever with repeat transfusion; however, leukocyte-poor red cells can be utilized
in patients with repetitive febrile nonhemolytic reactions.
Patients with IgA deficiency can exhibit more severe hypersensitivity reactions to transfusions, including rash and
anaphylaxis (Marino, pp. 702- 703).

Question 24

Which of the following laboratory tests is abnormally
prolonged with von Willebrand’s disease?
1. Prothrombin time
2. Partial thromboplastin time
3. Prothrombin 1: 1 dilution
4. Bleeding ti me

A. 1,2, and 3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 24

A. 1,2, and 3 are correct
B. 1 and3 are correct
**C. 2 and 4 are correct **
D. Only 4 is correct
E. All of the above are correct

Von ,Villebrand’s disease results in prolongations of
the partial thromboplastin time (PTI’) and bleeding time
because von Willebrand factor stabilizes factor VIII and
mediates platelet adhesion (Cecil, pp. 993).

Question 25

J\,Iatch the following shock syndromes with the
appropriate Swan-Ganz catheter measurements/vital signs,
using each answer once, more than once, or not at all. NoteCVP- central venous pressure (mm Hg), PCWP- pulmonary
capillary wedge pressure (m111 I-Ig) , CI- cardiac index
(L1mirlim2), SVR- systemic vascular resistance (dynes/cm2
)

CVP 16, PCWP 20, CI 1.2, SVR 1250
A. Hypovolemic shock
B. Cardiogenic shock
C. Septic shock

Answer 25

A. Hypovolemic shock
**B. Cardiogenic shock **
C. Septic shock

Hypovolemic shock is characterized by
decreased central venous and intracardiac pressures,
decreased cardiac output, elevated SVR (> 1200 dynes/cm2
),
and concomitant hypotension and tachycardia, with a
dampened Swan-Ganz catheter waveform. Cardiogenic shock
is characterized by a decreased cardiac index (less than
1.8 L/min/m2), elevated PCWP (> 18 mm Hg) and CVP, elevated SVR, and decreased systolic blood pressure « 100 mm
Hg). Septic shock is characterized by low filling pressures,
decreased SVR (although early septic shock can exhibit
an elevated SVR) , and normal or increased cardiac output.
Normal Swan-Ganz catheter parameters are as follows: CVP
1 to 6 mm Hg, PCWP 6 to 12 mm Hg, CI 2.4 to 4.0 Limin/nl,
SVR 900 to 1200 dynes/cm2 (Marino, pp. 164, 505-509).

Question 26

J\,Iatch the following shock syndromes with the
appropriate Swan-Ganz catheter measurements/vital signs,
using each answer once, more than once, or not at all. NoteCVP- central venous pressure (mm Hg), PCWP- pulmonary
capillary wedge pressure (m111 I-Ig) , CI- cardiac index
(L1mirlim2), SVR- systemic vascular resistance (dynes/cm2
)

CVP 4, PCWP 6, CI 4.5, SVR 350
A. Hypovolemic shock
B. Cardiogenic shock
C. Septic shock

Answer 26

A. Hypovolemic shock
B. Cardiogenic shock
C. Septic shock

Hypovolemic shock is characterized by
decreased central venous and intracardiac pressures,
decreased cardiac output, elevated SVR (> 1200 dynes/cm2
),
and concomitant hypotension and tachycardia, with a
dampened Swan-Ganz catheter waveform. Cardiogenic shock
is characterized by a decreased cardiac index (less than
1.8 L/min/m2), elevated PCWP (> 18 mm Hg) and CVP, elevated SVR, and decreased systolic blood pressure « 100 mm
Hg). Septic shock is characterized by low filling pressures,
decreased SVR (although early septic shock can exhibit
an elevated SVR) , and normal or increased cardiac output.
Normal Swan-Ganz catheter parameters are as follows: CVP
1 to 6 mm Hg, PCWP 6 to 12 mm Hg, CI 2.4 to 4.0 Limin/nl,
SVR 900 to 1200 dynes/cm2 (Marino, pp. 164, 505-509).

Question 27

J\,Iatch the following shock syndromes with the
appropriate Swan-Ganz catheter measurements/vital signs,
using each answer once, more than once, or not at all. NoteCVP- central venous pressure (mm Hg), PCWP- pulmonary
capillary wedge pressure (m111 I-Ig) , CI- cardiac index
(L1mirlim2), SVR- systemic vascular resistance (dynes/cm2
)

CVP 2, PCWP 5, CI 2.0, SVR 1400
A. Hypovolemic shock
B. Cardiogenic shock
C. Septic shock

Answer 27

**A. Hypovolemic shock **
B. Cardiogenic shock
C. Septic shock

Hypovolemic shock is characterized by
decreased central venous and intracardiac pressures,
decreased cardiac output, elevated SVR (> 1200 dynes/cm2
),
and concomitant hypotension and tachycardia, with a
dampened Swan-Ganz catheter waveform. Cardiogenic shock
is characterized by a decreased cardiac index (less than
1.8 L/min/m2), elevated PCWP (> 18 mm Hg) and CVP, elevated SVR, and decreased systolic blood pressure « 100 mm
Hg). Septic shock is characterized by low filling pressures,
decreased SVR (although early septic shock can exhibit
an elevated SVR) , and normal or increased cardiac output.
Normal Swan-Ganz catheter parameters are as follows: CVP
1 to 6 mm Hg, PCWP 6 to 12 mm Hg, CI 2.4 to 4.0 Limin/nl,
SVR 900 to 1200 dynes/cm2 (Marino, pp. 164, 505-509).

Question 28

Which of the following characteristics is NOT associated
with multiple endocrine neoplasia type 2 (Sipple syndrome) ?
A. Autosomal dominant inheritance
B. Pheochromocytomas
C. Pituitary adenomas
D. Medullary thyroid carcinoma
E. Parathyroid hyperplasia

Answer 28

A. Autosomal dominant inheritance
B. Pheochromocytomas
**C. Pituitary adenomas **
D. Medullary thyroid carcinoma
E. Parathyroid hyperplasia

j’vlultiple endocrine neoplasia (MEN) type 2 (Sipple
syndrome) is an autosomal dominant disorder that localizes
to chromosome 10 and is characterized by the development
pheochromocytomas and medullary thyroid carcinoma .
MEN-2 can be further subdivided into a type A (associated
with parathyroid hyperplasia or adenomas) and type B (associated with multiple mucosal neuromas). Pituitary adenomas
are associa ted with~lEN type 1 (Cecil, p. 1254).

Question 29

Which of the following characteristics are associated
with intraoperative venous air embolism?
1. High incidence in the sitting position
2. Most sensitive diagnostic modality is transesophageal
echocardiography
3. Associated with decreases in end tidal CO2
4. The pati ent should be placed rapidly in the right lateral
decubitus position
A. 1, 2, and3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 29

**A. 1, 2, and3 are correct **
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Intraoperative venous air embolism (VAE) has a high
incidence during procedures performed in the sitting position (up to 25 to 45% of all cases). VAE is characterized by
the development of bronchoconstriction, hypoxia , hypercarbia, hypotension, shock, cardiac arrhythmias, increased airway pressures, and decreased end-tidal CO2 (secondary to
increased dead space). Transesophageal echocardiography is
the most sensitive diagnostic modality for VAE, detecting
volumes as small as 0.02 mLlI\g of air entering the venous
system. The immediate treatment of suspected VAE entails
rapid hemostasis with concomitant irrigation of the surgical
field, lowering of the patient’s head with left lateral decubitus
positioning, increasing the Fi02 to 100%, stopping any concomitant nitrous oxide administration, manual occlusion of
the jugular veins, and aspiration of air from a multi orifice
CVP catheter (Greenberg, p. 602; Youmans, pp. 614- 615;
Wilkins, pp. 409-410).

Question 30

Select which of the following characteristics is most commonly observed with cerebral salt wasting/ syndrome of inappropriate ADH secretion (SIADH).
Hypovolemia
A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Answer 30

A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Cerebral salt wasting (CS,V) is
characterized by hyponatremia « 135) and hypovolemia
secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine
osmolality, decreased PCWP and CVP (hypovolemia), and
normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia
secondary to plasma volume expansion . SIADH is associated
with a deCi’eased serum osmolality « 280), i11creases in
urine sodium and osmolality levels (greater than plasma
osmolality), elevated PCWP and CVP (hypervolemia), and
normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be
observed in a delayed fashion with SlADH. The treatment
of SlADH is free water restriction, whereas the treatment of
CSW is volume and salt replacement. CSW can accompany
aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population ,
especially in the presence of vasospasm, to prevent the
delayed development of ischemic deficits (Youmans,
pp. 1829- 1830; Greenberg, pp. 17- 19).

Question 31

Select which of the following characteristics
is most commonly observed with cerebral salt wasting/
syndrome of inappropriate ADH secretion (SIADH).

Hypervolemia
A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Answer 31

A. Cerebral salt wasting
**B. SIADH **
C. Both of the above
D. None of the above

Cerebral salt wasting (CS,V) is
characterized by hyponatremia « 135) and hypovolemia
secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine
osmolality, decreased PCWP and CVP (hypovolemia), and
normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia
secondary to plasma volume expansion . SIADH is associated
with a deCi’eased serum osmolality « 280), i11creases in
urine sodium and osmolality levels (greater than plasma
osmolality), elevated PCWP and CVP (hypervolemia), and
normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be
observed in a delayed fashion with SlADH. The treatment
of SlADH is free water restriction, whereas the treatment of
CSW is volume and salt replacement. CSW can accompany
aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population ,
especially in the presence of vasospasm, to prevent the
delayed development of ischemic deficits (Youmans,
pp. 1829- 1830; Greenberg, pp. 17- 19).

Question 32

Select which of the following characteristics
is most commonly observed with cerebral salt wasting/
syndrome of inappropriate ADH secretion (SIADH).

Elevated serum osmolality
A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Answer 32

A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Cerebral salt wasting (CS,V) is
characterized by hyponatremia « 135) and hypovolemia
secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine
osmolality, decreased PCWP and CVP (hypovolemia), and
normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia
secondary to plasma volume expansion . SIADH is associated
with a deCi’eased serum osmolality « 280), i11creases in
urine sodium and osmolality levels (greater than plasma
osmolality), elevated PCWP and CVP (hypervolemia), and
normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be
observed in a delayed fashion with SlADH. The treatment
of SlADH is free water restriction, whereas the treatment of
CSW is volume and salt replacement. CSW can accompany
aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population ,
especially in the presence of vasospasm, to prevent the
delayed development of ischemic deficits (Youmans,
pp. 1829- 1830; Greenberg, pp. 17- 19).

Question 33

Select which of the following characteristics is most commonly observed with cerebral salt wasting/ syndrome of inappropriate ADH secretion (SIADH).
Hypouricemia
A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Answer 33

A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Cerebral salt wasting (CS,V) is
characterized by hyponatremia « 135) and hypovolemia
secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine
osmolality, decreased PCWP and CVP (hypovolemia), and
normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia
secondary to plasma volume expansion . SIADH is associated
with a deCi’eased serum osmolality « 280), i11creases in
urine sodium and osmolality levels (greater than plasma
osmolality), elevated PCWP and CVP (hypervolemia), and
normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be
observed in a delayed fashion with SlADH. The treatment
of SlADH is free water restriction, whereas the treatment of
CSW is volume and salt replacement. CSW can accompany
aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population ,
especially in the presence of vasospasm, to prevent the
delayed development of ischemic deficits (Youmans,
pp. 1829- 1830; Greenberg, pp. 17- 19).

Question 34

Select which of the following characteristics is most commonly observed with cerebral salt wasting/ syndrome of inappropriate ADH secretion (SIADH).
Treatment entails free water restriction
A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Answer 34

A. Cerebral salt wasting
B. SIADH
C. Both of the above
D. None of the above

Cerebral salt wasting (CS,V) is
characterized by hyponatremia « 135) and hypovolemia
secondary to renal sodium loss. CSW is associated with either normal or decreased serum osmolality « 280), elevated urine sodium levels (> 20 mEq/L), elevated urine
osmolality, decreased PCWP and CVP (hypovolemia), and
normal or elevated serum potassium levels. SIADII is characterized by the presence of hyponatremia and hypervolemia
secondary to plasma volume expansion . SIADH is associated
with a deCi’eased serum osmolality « 280), i11creases in
urine sodium and osmolality levels (greater than plasma
osmolality), elevated PCWP and CVP (hypervolemia), and
normal or decreased serum potassium levels. It is the presence of hypervolemia with SIADH that primarily distinguishes it from CSW, although hypouricemia tends to be
observed in a delayed fashion with SlADH. The treatment
of SlADH is free water restriction, whereas the treatment of
CSW is volume and salt replacement. CSW can accompany
aneurysmal subarachnoid hemorrhage and must be recognized and treated appropriately in this patient population ,
especially in the presence of vasospasm, to prevent the
delayed development of ischemic deficits (Youmans,
pp. 1829- 1830; Greenberg, pp. 17- 19).

Question 35

Which of the following agents is associated with the development of tension pneumocephalus?
A. Propofol
B. Isoflurane
C. Etomidate
D. Nitrous oxide
E. Lorazepam

Answer 35

A. Propofol
B. Isoflurane
C. Etomidate
D. Nitrous oxide
E. Lorazepam

Nitrous oxide increases cerebral blood flow and thus intracranial pressure when intracranial compliance is altered. Nitrous oxide can also diffuse into intracranial air faster than nitrogen can escape, which can contribute to the development of tension pneumocephalus (Greenberg,
p. 2; Youmans, p. 1508; Wilkins, p. 405).

Question 36

All of the following characteristics are associated with
barbiturates EXCEPT?
A. Dose-dependent EEG burst suppression
B. Associated with decreases in cerebral blood flow
C. Effects a re terminated primarily by redistribution
D. Can result in prominent peripheral vasoconstriction
E. Dose-dependent myocardial suppression

Answer 36

A. Dose-dependent EEG burst suppression
B. Associated with decreases in cerebral blood flow
C. Effects a re terminated primarily by redistribution
**D. Can result in prominent peripheral vasoconstriction **
E. Dose-dependent myocardial suppression

Barbiturates are anticonvulsants that result in prominent decreases in CBF and CMR02, dose-dependent EEG
burst suppression, dose-dependent myocardial suppression,
and peripheral vasodilation. Barbiturates are lipid-soluble
and their CNS effects are primarily terminated by redistribution. At higher dosages, barbiturates can actually result in
decreases in cerebral perfusion pressure if decreases in mean
arterial pressure exceed the decrease in intracranial pressure (Katzung, p. 410; Youmans, pp. 1508, 1521; Greenberg,
pp. 2, 776- 777; Will~ins, p. 404).

Question 37

Which of tbe following agents exhibits the highest selectivity for Beta l receptors?
A. Dobutamine
B. Dopamine
C. Epinephrine
D. Phenylephrine
E. Isoproterenol

Answer 37

A. Dobutamine
B. Dopamine
C. Epinephrine
D. Phenylephrine
E. Isoproterenol

See Table 7.37A. Dobutamine is relatively selective
for PI receptors, which makes it the agent of choice in the
treatment of severe systolic heart failure. Isoproterenol
is also a p-selective agent but has clinically insignificant
actions on (XI and (X2 receptors as well (Katzung, p. 128;
Marino, pp. 278-298; Greenberg, pp. 7- 9).

Question 38

Match the following metal intoxications with
their appropriate characteristics/therapies. Some answers
may be used once, more than once, or not at all:

Encephalopathy, peripheral neuropathy, hypochromic
anemia
A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Answer 38

A. Arsenic poisoning
**B. Lead pOisoning **
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Arsenic neuropathy is the most common of all the
heavy metal-induced neuropathies. Gastrointestinal (GI)
symptoms such as nausea, vomiting, and diarrhea occur
when large quantities are ingested, but these symptoms are
often absent if arsenic is taken parenterally or taken in small
amounts over a protracted period of time. In acute pOisoning,
the onset of symptoms usually takes 4 to 8 weeks to develop,
but the evolution of polyneuropathy is slower in chronic

Question 39

Match the following metal intoxications with
their appropriate characteristics/therapies. Some answers
may be used once, more than once, or not at all:

Gingivostomatitis, peripheral neuropathy, psychiatric
disturbances
A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Answer 39

A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Arsenic neuropathy is the most common of all the
heavy metal-induced neuropathies. Gastrointestinal (GI)
symptoms such as nausea, vomiting, and diarrhea occur
when large quantities are ingested, but these symptoms are
often absent if arsenic is taken parenterally or taken in small
amounts over a protracted period of time. In acute pOisoning,
the onset of symptoms usually takes 4 to 8 weeks to develop,
but the evolution of polyneuropathy is slower in chronic

Question 40

Match the following metal intoxications with
their appropriate characteristics/therapies. Some answers
may be used once, more than once, or not at all:

Treatment of choice for iron poisoning
A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Answer 40

A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
**H. Deferoxamine **
I. Manganese poisoning
J. None of the above

Arsenic neuropathy is the most common of all the
heavy metal-induced neuropathies. Gastrointestinal (GI)
symptoms such as nausea, vomiting, and diarrhea occur
when large quantities are ingested, but these symptoms are
often absent if arsenic is taken parenterally or taken in small
amounts over a protracted period of time. In acute pOisoning,
the onset of symptoms usually takes 4 to 8 weeks to develop,
but the evolution of polyneuropathy is slower in chronic

Question 41

Match the following metal intoxications with
their appropriate characteristics/therapies. Some answers
may be used once, more than once, or not at all:

Treatment of choice for lead poisoning in children
A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Answer 41

A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
**E. Succimer (DMSA) **
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Arsenic neuropathy is the most common of all the
heavy metal-induced neuropathies. Gastrointestinal (GI)
symptoms such as nausea, vomiting, and diarrhea occur
when large quantities are ingested, but these symptoms are
often absent if arsenic is taken parenterally or taken in small
amounts over a protracted period of time. In acute pOisoning,
the onset of symptoms usually takes 4 to 8 weeks to develop,
but the evolution of polyneuropathy is slower in chronic

Question 42

Match the following metal intoxications with
their appropriate characteristics/therapies. Some answers
may be used once, more than once, or not at all:

Cardiomyopathy, pancytopenia, hypotensive shock
A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Answer 42

**A. Arsenic poisoning **
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Arsenic neuropathy is the most common of all the
heavy metal-induced neuropathies. Gastrointestinal (GI)
symptoms such as nausea, vomiting, and diarrhea occur
when large quantities are ingested, but these symptoms are
often absent if arsenic is taken parenterally or taken in small
amounts over a protracted period of time. In acute pOisoning,
the onset of symptoms usually takes 4 to 8 weeks to develop,
but the evolution of polyneuropathy is slower in chronic

Question 43

Match the following metal intoxications with
their appropriate characteristics/therapies. Some answers
may be used once, more than once, or not at all:

Treatment of choice for Wilson’s disease
A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Answer 43

A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
**F. Penicillamine **
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Arsenic neuropathy is the most common of all the
heavy metal-induced neuropathies. Gastrointestinal (GI)
symptoms such as nausea, vomiting, and diarrhea occur
when large quantities are ingested, but these symptoms are
often absent if arsenic is taken parenterally or taken in small
amounts over a protracted period of time. In acute pOisoning,
the onset of symptoms usually takes 4 to 8 weeks to develop,
but the evolution of polyneuropathy is slower in chronic

Question 44

Match the following metal intoxications with
their appropriate characteristics/therapies. Some answers
may be used once, more than once, or not at all.

Sometimes treated with L-DOPA
A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
I. Manganese poisoning
J. None of the above

Answer 44

A. Arsenic poisoning
B. Lead pOisoning
C. Mercury poisoning
D. Iron poisoning
E. Succimer (DMSA)
F. Penicillamine
G. Thallium
H. Deferoxamine
**I. Manganese poisoning **
J. None of the above

Arsenic neuropathy is the most common of all the
heavy metal-induced neuropathies. Gastrointestinal (GI)
symptoms such as nausea, vomiting, and diarrhea occur
when large quantities are ingested, but these symptoms are
often absent if arsenic is taken parenterally or taken in small
amounts over a protracted period of time. In acute pOisoning,
the onset of symptoms usually takes 4 to 8 weeks to develop,
but the evolution of polyneuropathy is slower in chronic

Question 45

What is the maximum expected correction of a patient
with symptomatic hyponatremia over a 24-hour period
(mEq/L) ?
A. 4
B. 8
C. 12
D. 16
E. 20

Answer 45

A. 4
B. 8
C. 12
D. 16
E. 20

Symptomatic hyponatremia (generally < 125 mEq/L)
should be corrected at a Imudmal rate of 0.5 mEq/L/h (thus
12 mEq/L/24 h) to avoid central pontine myelinolysis
(Marino, p. 644; Greenberg, pp. 15- 16).

Question 46

At what point in time after injury does a healing wound
contain the maximum collagen content?
A. Two days
B. Two weeks
C. Two months
D. Two yea rs
E. None of the above

Answer 46

A. Two days
B. Two weeks
**C. Two months **
D. Two yea rs
E. None of the above

Wound healing occurs in primarily three phases: the
inflammatory, the proliferative, and the remodeling phases.
The inflammatory phase occurs during the first week and
is characterized by hemostasis as well as neutrophil and
macrophage infiltration. The proliferative phase occurs
from approximately 5 days to 3 weeks and consists of neovascularization, wound contraction (myofibroblasts), extracellular matri’i: synthesis (fibroblasts), and cellular migration
(epithelializa tion). The third phase (remodeling) occurs from
approximately 4 weeks to 2 years and consists of the aggregation and alignment of collagen fibers, with a progressive
increase in wound tensile strength for the first 6 to 8 months
until it plateaus. The wound contains the maximuIll collagen
content approximately 2 to 3 months after injury, during the
early portion of the proliferative phase (Robbins, pp. 74-76;
Will~ins, pp. 519- 520; Youmans, pp. 564-565).

Question 47

Which of the following anesthetics lower seizure
threshold?
1. Enflurane
2. Propofol
3. Methohexital
4. Diazepam

A. 1,2, and3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 47

A. 1,2, and3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Entlurane is an inhaled general anesthetic. that
actually lowers seizure threshold; methohexital is a barbiturate that also lowers seizure threshold. This property
renders these two agents unsuitable for most neurosurgical
procedures (Greenberg, pp. 2, 47; Katzung, p. 417; Youmans,
pp. 1508- 1512).

Question 48

A 34-year-old female presents with secondary amenorrhea, normal visual fields, and a prolactin level of 560 ng/mL.
The patient’s Mill showed evidence of an enhancing pituitary
macroadenorna, and she was initiated on oral bromocriptine
therapy. Over the subsequent several months the patient’s
prolactin level normalized, her macroadenoma decreased
significantly in size, and she eventually underwent a successful pregnancy. The patient was lost to follow up and then
presented acutely five years later with complaints of visual
loss. Repeat J’I’lRI showed a recurrent macroadenoma, and
the patient reported amenorrhea and galactorrhea. Routine
serum prolactin level was 39 ng/mL. What is the most likely
explanation for the patient’s current prolactin level?
A. Stalk effect
B. The macroadenoma no longer synthesizes prolactin
C. Hooll effect
D. Prior bromocriptine therapy favored the growth of
non-hormone-producing neoplastic pituitary cells
(null-cell adenoma)
E. None of the above

Answer 48

A. Stalk effect
B. The macroadenoma no longer synthesizes prolactin
**C. Hooll effect **
D. Prior bromocriptine therapy favored the growth of
non-hormone-producing neoplastic pituitary cells
(null-cell adenoma)
E. None of the above

The 1-1001, effect results in false-negative lab assays
for prolactin in the presence of extremely high prolactin
levels. This is secondary to inhibition of formation of the
normal prolactin-antibody complexes due to the presence
of extremely high prolactin levels. In these cases, a 1:100
prolactin dilution should be obtained to effectively rule
out a prolactinoma. Stalk effect results from compression
of the adjacent hypothalamus or pituitary stalk by nonprolactin-secreting m<lcroadenomas and commonly results
in prolactin levels of 25 to 150 ng/mL. Pituitary adenomas
are typically monoclonal neoplasms; thus it is unlikely that a
null cell adenoma has arisen in a patient with a prior Imown
prolactinoma. The diagnosis of a prolactinoma generally requires a serum prolactin level of > 200 ng/mL (Greenberg,
pp. 420- 426; Kaye and Laws, pp. 206- 210).

Question 49

All of the following characteristics are consistent with
the high-dose dexamethasone suppression test (2 mg q 6 h x
8 doses) EXCEPT?
A. Distinguishes Cushing’s disease from cortisol-producing
adrenal adenomas
B. Urine free cortisol levels will exhibit 90% suppression
of baseline wi th Cushing’s disease
C. 17 -Ilydroxysteroids are suppressed to < 50% of baseline with Cushing’s disease
D. Adrenal adenomas exhibit 25 to 50% suppression of
urine free cortisol baseline levels
E. None of the above

Answer 49

A. Distinguishes Cushing’s disease from cortisol-producing
adrenal adenomas
B. Urine free cortisol levels will exhibit 90% suppression
of baseline wi th Cushing’s disease
C. 17 -Ilydroxysteroids are suppressed to < 50% of baseline with Cushing’s disease
**D. Adrenal adenomas exhibit 25 to 50% suppression of
urine free cortisol baseline levels **
E. None of the above

The high-dose dexamethasone suppression test
helps distinguish Cushing’s disease (ACTH-secreting pituitary adenoma) from ectopic sources of ACTH and cortisolproducing adrenal adenomas. Pituitary adenomas will
exhibit suppression with this test, with concomitant
deCI’eases in 17 -hydroxysteroids to < 50% of baseline and
urine free cortisol levels to < 90% of baseline. Adrenal
adenomas are ACTI-I-independent and thus do not respond
to the high-dose dexamethasone suppression test (Cecil,
p.1217; Youmans, pp. 1196-1197).

Question 50

50. Which of the following characteristics is consistent with
    induced barbiturate coma in patients with closed head
    injuries?
51. Adequa te burst suppression on EEG is associated with
    maximal reductions in cerebral metabolism (CJ’vIR02)
52. Barbiturates improve global cerebral perfusion
53. Barbiturates can result in myocardial depression
54. Barbiturates are associated with immunosuppression

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 50

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
**E. All of the above are correct **

High-dose barbiturates uncouple cerebral blood flow
and cerebral metabolism, thus resulting in decreases in
CMROz and increases in CBF. Burst suppression on EEG
results in maximal reductions in CMROz with continuous
barbiturate infusions. JIigh-dose barbiturate therapy is associated with myocardial depression and hypotension, and
patients often require concomitant vasopressor therapy to
maintain an adequate mean arterial pressure during barbiturate infusions. Other effects of high-dose barbiturat infusion include inmmnosuppression, impaired gastric
motility, increased lysosomal stability, and improved freeradical scavenging. Global cerebral perfusion is improved
with barbiturate infusions, and it is thought that blood is
“shunted” from normal brain regions to damaged (ischemic)
regions. Although barbiturate infusions can lower ICP,
improvements in overall outcomes in patients with closed
head injuries undergoing high-dose barbiturate therapy is
controversial (Greenberg, pp. 653- 654; Will~ins, p. 353).

Question 51

Which of the following should be utilized in the treatment
of coagulopathy resulting from von Willebrand’s disease?
1. Fresh frozen plasma
2. Desmopressin
3. Platelets
4. Cryoprecipitate

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 51

A. 1,2, and 3 are correct
B. 1 and 3 are correct
**C. 2 and 4 are correct **
D. Only 4 is correct
E. All of the above are correct

Von \Villebrand’s disease (VWD) results in prolongation of the partial thromboplastin time (PTT) and bleeding
time. Coagulopathy resulting from VWD is typically treated
with cryoprecipitate, which is rich in both factor VIII and
von Willebrand factor as well as desmopressin (DDAVP),
which facilitates the release of von Willebrand factor from
epithelial cells (Ceci l, p. 994)

Question 52

Which of the follOWing characteristics is NOT associated
with perioperative gastrointestinal bleeding?
A. Patients with severe closed head injuries
B. Patients with> 30% body surface area burns
C. Hypotensive shock
D. Early postoperative enteral feeds
E. Incidence is deCl’eased with utilization of H2 blockers
and sucralfate

Answer 52

A. Patients with severe closed head injuries
B. Patients with> 30% body surface area burns
C. Hypotensive shock
D. Early postoperative enteral feeds
E. Incidence is deCl’eased with utilization of H2 blockers
and sucralfate

Superficial stress ulcers in the gastric/duodenal
mucosa are a result of regional decreases in blood flow and
are exacerbated by the presence 0fI-1+. Patients in the highest
risk category for GI hemorrhages are those with severe
closed head injuries (Cushing’s ulcer) and those with burns
over> 30% body surface area (Curling’s ulcer). Superficial
stress ulcers can lead to nosocomial sepsis and occult GI
bleeding, although overt hemorrhage occurs in only 5% of all
cases of stress ulcers. The risk of perioperative GI bleeding
can be decreased with the administration of H2 blockers and
sucralfate, maintenance of adequate systemic blood pressure
and oxygen transport, and initiation of early enteral feedings
(Marino, pp. 94- 101).

Question 53

Which of the following acute phase reactants are typically increased during periods of acute systemic inflammation?
1. C-reac tive protein
2. Fibrinogen
3. Haptoglobin
4. Al bumin

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 53

**A. 1,2, and 3 are correct **
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Acute-phase reactants are a group of proteins that
are largely synthesized by the liver. Synthesis of the acutephase reactants is altered during periods of systemic
inflammation, which results in prominent increases in
several plasma proteins including C-reactive protein, serum
amyloid A, fibrinogen, von Willebrand factor, ai-antitrypsin,
haptoglobin, ceruloplasmin, and several complement proteins. Serum plasma levels of albumin and transferrin are
typically decreased during periods of acute inflammation
(Cecil, pp. 1535-1537).

Question 54

Which of the following agents act as pyrogens at the
hypothalamus?
1. Interleukin-6
2. Tumor necrosis factor
3. Interleukin-1
4. Prostaglandin E2

A. 1, 2, and 3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 54

A. 1, 2, and 3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

There are several different proteins that act at the
anterior hypothalamus to induce a systemic fever (pyrogens), including interleukin-l, interleukin-6, tumor necrosis
factor, interferon-a, and some bacterial toxins. All of these
substances induce local increases in prostaglandin E2 levels
in the anterior hypothalamus to increase the temperature set
point (Ceci l, pp. 1533-1535).

Question 55

Which of the following parameters is the best indicator of
adequa te tissue perfusion?

A. Systolic blood pressure
B. Urine output
C. Heart rate
D. Gastrointestinal pH
E. Oxygen saturation

Answer 55

A. Systolic blood pressure
B. Urine output
C. Heart rate
**D. Gastrointestinal pH **
E. Oxygen saturation

In shock states, blood is selectively shunted away
from the GI tract, which results in decreases in the local
gastric pH. GI pH normalizes after adequate resuscitation
and is thus an excellent indicator of regional perfusion. Normal systolic blood pressure, heart rate , and even urine
output can all be observed in inadequately resuscitated
patients who are in states of compensated shock (Marino,
pp. 198-200; Brown et aI., pp. 569- 585).

Question 56

Which of the following features is NOT typically associated with septic shock?

A. ,tl’lelltal status changes
B. Respiratory acidosis
C. Hyperglycemia
D. Increased pulse pressure
E. Elevated white blood cell count

Answer 56

A. ,tl’lelltal status changes
**B. Respiratory acidosis **
C. Hyperglycemia
D. Increased pulse pressure
E. Elevated white blood cell count

Septic shock is usually a result of bacteremia with
gram-positive or gram-negative organisms, although it can
also occur with fungal and anaerobic infections. Septic shock
often exhibits fever, mental status changes, tachypnea,
tachycardia, an increased pulse pressure, hyperglycemia,
and an elevated white blood cell count. Septic shock results
in tachypnea and a concomitant respiratory alkalosis early
in the disease course, although late in the disease course a
concomitant metabolic acidosis can occur from lactate accumulation (hypoperfusion). Septic shock is also accompanied
by tachycardia and an increased cardiac output initially,
although cardiac output and stroke volume are often decreased
in the later stages of septic shock. i\·lost patients with sepsis
exhibit an elevated white blood cell count and hyperglycemia
(glucocorticoid release), although marked decreases in the
white blood cell count and hypoglycemia (with prominent
bacteremia) are also occasionally observed (Marino, pp. 505-
510).

Question 57

Which of the following me tabolic complications is
NOT typically associated with the administration of total
parenteral nutrition?
A. Hyperglycemia
B. Essential fatty acid deficiency
C. Metabolic alkalosis
D. Hypophosphatemia
E. Hepatic cholestasis

Answer 57

A. Hyperglycemia
B. Essential fatty acid deficiency
**C. Metabolic alkalosis **
D. Hypophosphatemia
E. Hepatic cholestasis

Metabolic complications of total parentej’al nutrition
(TPN) include volume overload, hyperglycemia, hypophosphatemia, hyperchloremic metabolic acidosis, hypomagnesemia, hypokalemia, trace element defiCiency, and
essential fatty acid defiCiency. Patients on long-term TPN
are also at risk to develop hepatic cholestasis and vitamin
deficiencies. Other complications of TPN include complications related to central line placement (e.g., pneumothorax,
hemothorax) and the presence of an indwelling central
catheter (e.g. , venous thrombosis mid sepsis) (Marino,
pp. 759- 763).

Question 58

Which of the following characteristics are consistent
with pseudomembranous colitis?
1. Prior antibiotic administration
2. Development of toxic megacolon
3. Watery diarrhea
4. Enzyme-linked immunosorbent assays (ELISA) for C.
dijJicile toxins represent the gold standard in laboratory diagnosis
A. 1, 2, a nd 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 58

**A. 1, 2, a nd 3 are correct **
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Pseudomembranous colitis (PMC) is a relatively
common cause of severe diarrhea and colitis in the ICU
population and results from toxins produced by ClostricUu’/1l
di((icile. PMC is usually associated with prior exposure to
third-generation cephalosporins, clindamycin, or one of the
penicillins, although many different antibiotics have been
implicated in the development of this disorder. C. di/ficile
produces two different toxins (tOxin A and toxin B) that
ultimately result in disruption of colonic mucosal integrity,
with subsequent fluid secretion, inflammation, and edema.
Findings of PMC include fever, leukocytosis, watery diarrhea ,
abdominal pain/cramping, dehydration, hypoalbuminemia,
and even the development of sepsis and toxic megacolon
(with colonic perforations). The “gold standard” laboratory
study for the diagnosis of PMC is direct cytotoxic assay of
stool filtrate for C. dij]icile toxin. ELISA tests for C. ditficile
toxin are also available; however, they exhibit low sensitivity. Direct culture of the bacterium is the most sensitive
laboratory assay, but it is rarely performed due to time and cost constraints and the inability to differentiate between
normal and toxic strains of c. ditncile. The treatment of PMC
includes discontinuation of causative antibiotics, fluid and
electrolyte repletion, aod the admiJlistration of oral metronidazole (Flagyl) (Marino, pp. 534-537).

Question 59

Which of the following studi es has the highest positive
predictive value in the diagnosis of acute pulmonary
embolism?
A. Pulmonary angiogram
B. High resolution helical computed tomographic angiography
C. Nuclear scintigraphic ventilation-perfusion lung scan
D. Venous duplex ultrasound
E. None of the above

Answer 59

**A. Pulmonary angiogram **
B. High resolution helical computed tomographic angiography
C. Nuclear scintigraphic ventilation-perfusion lung scan
D. Venous duplex ultrasound
E. None of the above

Pulmonary angiography continues to be the gold
standard in the diagnosis of acute pulmonary embolism (PE),
with close to a 100% positive predictive value and 90% negative predictive value. High-resolution helical CT angiography
is evolving as a more accurate diagnostic modality for acute
pulmonary embolism, although its sensitivity and specificity
are not as well defined. Nuclear scintigraphic ventilationperfusion (V/Q) lung scan is often the initial diagnostic study
of choice in patients with small pulmonary emboli, although
approximately 40% of all patients with an acute PE will
exhibit a nondiagnostic (indeterminate) V/Q scan. Lower
extremity duplex ultrasound can often confirm the source of
a PE, although a negative result does not significantly reduce
the likelihood of a PE (Marino, pp. 112-115).

Question 60

Warfarin (Coumadin) administration inhibits synthesis
of which of the following clotting factors/anticoagulant
proteins?
1. Factor VII
2. Factor II
3. Factor IX
4. Protein C

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 60

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
**E. All of the above **

Warfarin (Coumadin) inhibits the synthesis of the
vitamin K-dependent clotting factors (factors II, VII, L,{, X)
and the anticoagulant proteins C and S (Katzung, p. 552).

Question 61

\Vhich of the following medications can result in a decrease
in the bioavailability of warfarin during coadministration?
1. Barbiturates
2. Cimetidine
3. Rifampin
4. Metronidazole

A. 1, 2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 61

A. 1, 2, and 3 are correct
**B. 1 and 3 are correct **
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Barbiturates, rifampin, and cholestyramine admirlistration can all result in decreased levels of warfarin
(and thus decreases in u\TR). Cimetidine, metronidazole,
trimethoprim-sulfamethoxazole, fluconazole, amiodarone,
and disulfiram all result in increased levels of coumadin (and
thus increases in INR) (Katzung, p. 554).

Question 62

Which of the following characteristics is NOT observed
with primary aldosteronism (Conn’s syndrome)?
A. Hypertension
B. Hyperkalemia
C. Low plasma renin activity
D. Metabolic alkalosis
E. IIypomagnesemia

Answer 62

A. Hypertension
**B. Hyperkalemia **
C. Low plasma renin activity
D. Metabolic alkalosis
E. IIypomagnesemia

Primary aldosteronism (Conn’s syndrome) is characterized by hypertension , hypernatremia, hypokalemia,
metabolic alkalosis, and low plasma renin activity. Excessive
aldosterone levels promote retention of sodium, water, and
bicarbonate in the distal renal tubules, with concomitant
losses of potassium and magnesium. The majority of cases
of Conn’s syndrome result from excessive production of
aldosterone by an adrenal adenoma (Cecil , p. 1249).

Question 63

A 22-year-old male is brought to the emergency department after sustaining injuries in a motor vehicle collision.
The patient has a heart rate of 122, respiratory rate of 28,
systolic blood pressure of 86, oxygen saturation of 88%, and
mild tracheal deviation to the left. What is the immediate
next step in management of this condition?
A. Emergent needle thoracocentesis
B. Placement of a thoracostomy tube
C. Portable chest x-ray
D. Obtain an arterial blood gas
E. CT scan of the chest

Answer 63

**A. Emergent needle thoracocentesis **
B. Placement of a thoracostomy tube
C. Portable chest x-ray
D. Obtain an arterial blood gas
E. CT scan of the chest

Tension pneumothorax is a life-threatening condition
tha t often exhibits tracheal deviation to the side opposite the
pneumothorax. The marked increases in intrathoracic pressure that accompany tension pneumothorax can result in
prominent decreases in venous blood return to the heart,
with concomitant hypotension and shock, as in this case.
ATLS guidelines recolllmend immediate empiric treatment
of suspected tension pneumothorax with needle thoracocentesis, followed by placement of a definitive thoracostomy
tube (American College of Surgeons Committee on Trauma,
pp. 128-129).

Question 64

A 46-year-old male with no prior surgical history
is intubated and placed under general anesthesia for an elective anterior cervical discectomy and fusion. Shortly after
intubation, the patient exhibits a prominent increase in end
tidal CO2 , tachycardia, and an elevated temperature.

What is the immediate next step in management?
A. STAT portable chest x-ray
B. Immediate cessation of inhala tional anesthetics
C. Heparin anticoagulation
D. Increase in ventilatory rate
E. None of the above

Answer 64

A. STAT portable chest x-ray
**B. Immediate cessation of inhala tional anesthetics **
C. Heparin anticoagulation
D. Increase in ventilatory rate
E. None of the above

lvIalignant hyperthermia is a heritable disorder that is characterized by skeletal muscle hype tabolism secondary to decreased calcium sequestration
in the sarcoplasmic reticulum. Malignant hyperthermia is
associated with the administration of SUCCinylcholine and
some inhalational anesthetics (e.g. , halothane, cyclopropane).
This disorder is characterized by the acute onset of an
increase in end-tidal CO2 , tachycardia, muscle rigidity, and
an elevated temperature. With disease progression, arrhythmias, hypoxia , metabolic acidoSiS, pulmonary edema,
disseminated intravascular coagulation, rhabdomyolysis,
hypotension, and even cardiac arrest can occur. The mortality of malignant hyperthermia is as high as 30%. Suspected
cases should be treated initially by the immediate cessation
of the suspected offending agent, followed by the administration of IV dantrolene until symptoms cease (Greenberg,
pp.4- 5).

Question 65

A 46-year-old male with no prior surgical history
is intubated and placed under general anesthesia for an elective anterior cervical discectomy and fusion. Shortly after
intubation, the patient exhibits a prominent increase in end
tidal CO2 , tachycardia, and an elevated temperature.

Which of the following features are likely to develop with
delays in diagnosis and treatment of the above malady?
1. Hypoxia
2. Metabolic acidosis
3. Rhabdomyolysis
4. Disseminated intravascular coagulation

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 65

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and4 are correct
D. Only 4 is correct
**E. All of the above are correct **

lvIalignant hyperthermia is a heritable disorder that is characterized by skeletal muscle hype tabolism secondary to decreased calcium sequestration
in the sarcoplasmic reticulum. Malignant hyperthermia is
associated with the administration of SUCCinylcholine and
some inhalational anesthetics (e.g. , halothane, cyclopropane).
This disorder is characterized by the acute onset of an
increase in end-tidal CO2 , tachycardia, muscle rigidity, and
an elevated temperature. With disease progression, arrhythmias, hypoxia , metabolic acidoSiS, pulmonary edema,
disseminated intravascular coagulation, rhabdomyolysis,
hypotension, and even cardiac arrest can occur. The mortality of malignant hyperthermia is as high as 30%. Suspected
cases should be treated initially by the immediate cessation
of the suspected offending agent, followed by the administration of IV dantrolene until symptoms cease (Greenberg,
pp.4- 5).

Question 66

A 46-year-old male with no prior surgical history
is intubated and placed under general anesthesia for an elective anterior cervical discectomy and fusion. Shortly after
intubation, the patient exhibits a prominent increase in end
tidal CO2 , tachycardia, and an elevated temperature.

Administration of what medication is effective in halting
the progression of the above disorder in the majority of
cases?
A. Propofol
B. Etomidate
C. Lorazepam
D. Dantrolene
E. Heparin

Answer 66

A. Propofol
B. Etomidate
C. Lorazepam
**D. Dantrolene **
E. Heparin

lvIalignant hyperthermia is a heritable disorder that is characterized by skeletal muscle hype tabolism secondary to decreased calcium sequestration
in the sarcoplasmic reticulum. Malignant hyperthermia is
associated with the administration of SUCCinylcholine and
some inhalational anesthetics (e.g. , halothane, cyclopropane).
This disorder is characterized by the acute onset of an
increase in end-tidal CO2 , tachycardia, muscle rigidity, and
an elevated temperature. With disease progression, arrhythmias, hypoxia , metabolic acidoSiS, pulmonary edema,
disseminated intravascular coagulation, rhabdomyolysis,
hypotension, and even cardiac arrest can occur. The mortality of malignant hyperthermia is as high as 30%. Suspected
cases should be treated initially by the immediate cessation
of the suspected offending agent, followed by the administration of IV dantrolene until symptoms cease (Greenberg,
pp.4- 5).

Question 67

Which of the following is effective in the treatment of
hyperca lcemia ?
1. Furosemide
2. Isotonic saline
3. Calcitonin
4. Pamidronate

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct

Answer 67

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
**E. All of the above are correct **

Hypercalcemia is quite rare in the ICU setting and is
usually secondary to the presence of hyperparathyroidism,
thyrotoxicosis, or malignancy. Medications that are effective in the treatment of hypercalcemia include furosemide
(promotes urinary excretion), isotonic saline (corrects
hypovolemia and promotes calcium excretion), calcitonin
(inhibits bone resorption), hydrocortisone, bisphosphonates (e.g., pamidronate), and plicamycin (mithramycin).
Hemodialysis is also an effective treatment for hypercalcemia (Marino, pp. 679- 681).

Question 68

Which of the following characteristics are consistent
with fat embolism?
1. Global cerebral dysfunction
2. Renal dysfunction
3. Conjunctival petechiae
4. Treatment involves avoidance of positive pressure
ven tila tion

A. 1,2, and3 are correct
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 68

**A. 1,2, and3 are correct **
B. 1 and3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Fat embolism is characterized by pulmonary, cerebral, hepatic, and renal involvement. Cerebral symptoms are
usually global, and pulmonary symptoms usually dominate
the clinical presentation. Occasionally petechiae of the
chest and conjunctivae are observed . Treatment entails
aggressive oxygenation with positive-pressure ventilation,
volume resuscitation, and the administration of corticosteroids (Robbins, pp. 110-111; Will~ins, pp. 2704-2705).

Question 69

Which of the following pathogens are most likely to cause
early (less than 2 weeks) and late (greater than 6 months)
shunt infections, respectively?
A. Staph. alirellS, Staph. epidennidis
B. Staph. epidermiclis, Strep. pnewllonia
C. Staph. epidernl’idis, Staph. epidennidis
D. Staph. epidennidis, P. acnes
E. Staph. epidenniciis, Staph. [t.ltreliS

Answer 69

A. Staph. alirellS, Staph. epidennidis
B. Staph. epidermiclis, Strep. pnewllonia
**C. Staph. epidernl’idis, Staph. epidennidis **
D. Staph. epidennidis, P. acnes
E. Staph. epidenniciis, Staph. [t.ltreliS

Staphylococclls epiden11’idis is the most com111on
pathogen to result in shunt infections in both an early and
late fashion (Greenberg, p. 214).

Question 70

Match the following anesthetic agents with their most appropriate characteristic. Some letters may be used once, more than once, or not at all. Increases both cerebral metabolism and cerebral blood flow
A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Answer 70

A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and
ICP. Etomidate can also suppress cortisol synthesis with prolonged infusions. IIalothane is an inhalational anesthetic
that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation, all of which can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CEF. Barbiturates also exhibit minimal effects
upon evoked potentials (Greenberg, pp. 1-3; Katzung, pp. 417, 420-422).

Question 71

Match the following anesthetic agents with their
most appropriate characteristic. Some letters may be used
once, more than once, or not at all.

Markedly increases CBF and can disrupt autoregulation
A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Answer 71

A. Etomidate
B. Propofol
C. Lorazepam
**D. Halothane **
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is
a potent cerebral vasoconstrictor that reduces CBF and
ICP. Etomidate can also suppress cortisol synthesis with
prolonged infusions. IIalothane is an inhalational anesthetic
that increases CBF (often as high as 100%), decreases CSF
absorption, and disrupts autoregulation, all of which can
contribute to elevated ICP. Nitrous oxide increases both
CBF and cerebral metabolism and increases the risk of
developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general
increase CSF absorption and decrease cerebral metabolism.
Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism
and increase CEF. Barbiturates also exhibit minimal effects
upon evoked potentials (Greenberg, pp. 1-3; Katzung,
pp. 417, 420-422).

Question 72

Match the following anesthetic agents with their
most appropriate characteristic. Some letters may be used
once, more than once, or not at all.

Reduces cerebral metabolism and increases CSF
absorption
A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Answer 72

A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
**G. Fentanyl **
H. Pentobarbital
I. None of the above

Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is
a potent cerebral vasoconstrictor that reduces CBF and
ICP. Etomidate can also suppress cortisol synthesis with
prolonged infusions. IIalothane is an inhalational anesthetic
that increases CBF (often as high as 100%), decreases CSF
absorption, and disrupts autoregulation, all of which can
contribute to elevated ICP. Nitrous oxide increases both
CBF and cerebral metabolism and increases the risk of
developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general
increase CSF absorption and decrease cerebral metabolism.
Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism
and increase CEF. Barbiturates also exhibit minimal effects
upon evoked potentials (Greenberg, pp. 1-3; Katzung,
pp. 417, 420-422).

Question 73

Match the following anesthetic agents with their
most appropriate characteristic. Some letters may be used
once, more than once, or not at all.

Reduces CBF and JCP, suppresses cortisol production
with prolonged infusions
A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Answer 73

**A. Etomidate **
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is
a potent cerebral vasoconstrictor that reduces CBF and
ICP. Etomidate can also suppress cortisol synthesis with
prolonged infusions. IIalothane is an inhalational anesthetic
that increases CBF (often as high as 100%), decreases CSF
absorption, and disrupts autoregulation, all of which can
contribute to elevated ICP. Nitrous oxide increases both
CBF and cerebral metabolism and increases the risk of
developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general
increase CSF absorption and decrease cerebral metabolism.
Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism
and increase CEF. Barbiturates also exhibit minimal effects
upon evoked potentials (Greenberg, pp. 1-3; Katzung,
pp. 417, 420-422).

Question 74

Match the following anesthetic agents with their
most appropriate characteristic. Some letters may be used
once, more than once, or not at all.

Uncouples CBF and cerebral me tabolism, minimal
effects on evoked potentials
A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
H. Pentobarbital
I. None of the above

Answer 74

A. Etomidate
B. Propofol
C. Lorazepam
D. Halothane
E. Isoflurane
F. Nitrous oxide
G. Fentanyl
**H. Pentobarbital **
I. None of the above

Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is
a potent cerebral vasoconstrictor that reduces CBF and
ICP. Etomidate can also suppress cortisol synthesis with
prolonged infusions. IIalothane is an inhalational anesthetic
that increases CBF (often as high as 100%), decreases CSF
absorption, and disrupts autoregulation, all of which can
contribute to elevated ICP. Nitrous oxide increases both
CBF and cerebral metabolism and increases the risk of
developing tension pneumocephalus in patients with underlying pneul11ocephalus. Narcotics (e.g. , fentanyl) in general
increase CSF absorption and decrease cerebral metabolism.
Barbiturates (e.g., pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism
and increase CEF. Barbiturates also exhibit minimal effects
upon evoked potentials (Greenberg, pp. 1-3; Katzung,
pp. 417, 420-422).

Question 75

An 18-year-old male suffers a moderate closed head
injury with a concomitant fracture of the skull base. The
patient exhibits prominent meningeal signs with a fever
and leukocytosis one week after the injury. Which of the
following organisms is the most likely to be identified on
CSF culture?
A. Haemophihls’i11flllenzae
B. Mora ~e lla catarrhaNs
C. Strep. ]Jneumoniae
D. ]({ebsiella pneumonia
E. Staph. epidennidis

Answer 75

A. Haemophihls’i11flllenzae
B. Mora ~e lla catarrhaNs
C. Strep. ]Jneumoniae
D. ]({ebsiella pneumonia
E. Staph. epidennidis

Streptococcus pllewl10niCle is associated with approximately SO to 70% of all cases of meningitis occurring
after traumatic skull fractures. lVter the appropriate antibiotics are administered and the patient recovers from
meningitis, a thorough evaluation for the presence of a CSF
fistula, with possible surgical repair, should be entertained
(Will<ins, p. 3305; Greenberg, p. 213).

Question 76

Which of the following side effects is NOT typically
associated with administration of BCl\TU (carmustine)?
A. Interstitial pneumonitis
B. Hepatitis
C. Bone marrow suppression
D. Nausea
E. Hemorrhagic cystitis

Answer 76

A. Interstitial pneumonitis
B. Hepatitis
C. Bone marrow suppression
D. Nausea
E. Hemorrhagic cystitis

BCl\TU is associated with alopecia, bone marrow
suppression, dysphagia, encephalopathy, nausea, diarrhea,
hepatitis, and renal failure. Some of the most important side
effects of BCl\TU are dose-dependent pulmonary complications, including interstitial pneumonitis and pulmonary
fibrosis (Katzung, pp. 888-889).

Question 77

Which of the following agents is most appropriate for the
treatment of urinary retention?
A. Oxybutynin
B. Bethanecol
C. Imipramine
D. Atropine
E. Methacholine

Answer 77

A. Oxybutynin
**B. Bethanecol **
C. Imipramine
D. Atropine
E. Methacholine

Bethanechol is a muscarinic agonist that facilitates
detrusor contraction and inhibits contraction of the bladder
sphincter and trigone, thus effectively treating urinary retention . Methacholine is also a muscarinic agonist, however, it
is typically used to facilitate the diagnosis of hyperactive
airway disease (e.g. , asthma) due to its potent bronchoconstrictive effects (Greenberg, p. 116; Katzung, pp. 94, 96, 100).

Question 78

Which of the following is most likely to account for
cases of nosocomial pneumonia in patients on mechanical
ventilation?
A. Gram-positive cocci
B. Gram-positive rods
C. Gram-negative cocci
D. Gram-negative rods
E. None of the above

Answer 78

A. Gram-positive cocci
B. Gram-positive rods
C. Gram-negative cocci
**D. Gram-negative rods **
E. None of the above

While gram-positive cocci (e.g., Streptococcus plleu.-
moniC/e) account for the majority of cases of coml11unityacquired pneumonias, gram-negative rods account for the
majority of cases of nosocomial pneumonia. Gram-negative
rods account for 46% of all cases of nosocomial pneumonia in
ward patients and 83% of all patients on mechanical ventilation. PseudomollCls species are the most common bacteria to
account for ventilator-associated nosocomial pneumonia
(30% of all cases) (Marino, pp. 516-517).

Question 79

Which of the following characteristics are consistent
with disseminated intravascular coagulation (DIC)?
1. Associated with diffuse microvascular thrombosis
2. Associated with widespread release of tissue factor
3. Often results in fulminant ARDS
4. Heparin is contraindicated with onset of DIC

A. 1, 2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 79

**A. 1, 2, and 3 are correct **
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

DIC is often a result of sepsis and severe systemic
trauma, which results in endothelial cell damage and release
of tissue factor. The presence of large amounts of tissue factor can result in the diffuse activation of both the fibrinolytic
and coagulation pathways. Clinically, DIC is characterized
by diffuse microvascular thrombosis, thrombocytopenia,
and hemorrhage (especially GI bleeding). As DIC progresses,
oliguric renal failure, ARDS, and even death from multiple
organ failure can ensue. DIC often exhibits elevations of
fibrin split products (D-dimer), decreases in fibrinogen, prolongations of the PT and PTT, and thrombocytopenia.
Although not contraindicated, heparin is often ineffective
in controlling the diffuse microvascular thrombosis that is
inherent to DIC because antithrombin III levels are concomitantly decreased (Marino, pp. 712-713).

Question 80

Which of the following agents has been associated with
precipitating thyrotoxicosis (Jodbasedow effect)?
A. Iodinated radiographic contrast dye
B. Propylthiouracil
C. Hydrocortisone
D. Propranolol
E. None of the above

Answer 80

**A. Iodinated radiographic contrast dye **
B. Propylthiouracil
C. Hydrocortisone
D. Propranolol
E. None of the above

The 10dbasedow effect refers to the precipitation
of thyrotoxicosis in patients with toxic nodular goiter (or
occasionally Graves’ disease) who are exposed to large levels of iodine acutely. Common precipitating agents include
iodinated radiographic contrast dye and amiodarone (Cecil,
pp.1235- 1236).

Question 81

Which of the following paralytics is associated with the development of hyperkalemia?
A. Rocuronium
B. Vecuronium
C. Pancuronium
D. Succinylcholine
E. None of the above

Answer 81

A. Rocuronium
B. Vecuronium
C. Pancuronium
D. Succinylcholine
E. None of the above

Succinylcholine usually results in mild elevations in serum potassium levels and is rarely associated with severe hyperkalemia (Greenberg, p. 49; Katzung, p. 444).

Question 82

Which of the following vitamins is often coadministered
with isoniazid to prevent a relative deficiency?
A. Thiamine
B. Vitamin K
C. Pyridoxine
D. Vitamin B12
E. Vitamin D

Answer 82

A. Thiamine
B. Vitamin K
**C. Pyridoxine **
D. Vitamin B12
E. Vitamin D

Isoniazid is associated with the development of
peripheral neuropathy that occurs secondary to a relative
pyridoxine defiCiency (excessive excretion). Administration
of pyridoxine during isoniazid therapy is effective in preventing the development of peripheral neuropathy (Katzung,
p. 773).

Question 83

Which of the following is NOT characteristic of atropine
toxicity?
A. Mydriasis
B. Xerostomia
C. Delirium
D. Bradycardia
E. Cutaneous flushing

Answer 83

A. Mydriasis
B. Xerostomia
C. Delirium
**D. Bradycardia **
E. Cutaneous flushing

Atropine is an antimuscarinic agent that blocks
almost all parasympathetic effects at high concentrations.
Symptoms of atropine toxicity include delirium, mydriasis,
cycloplegia , xerostomia, tachycardia , cutaneous flushing,
and fever. Treatment of atropine toxicity involves the judicious use of physostigmine (Katzung, pp. 113-114).

Question 84

A 56-year-old male complains of severe chest pain on postoperative day 1 after undergoing elective lumbar microdiscectomy. The patient’s blood pressure is 163/82 with a pulse of 48, respiratory rate of 18, and oxygen saturation of 98% on 2 L of oxygen via nasal cannula. The patient’s ECG shows evidence of ST elevations of 0.5 to 2.0 mm in three successive leads. Which of the following medications should be administered (i.e., are NOT contraindicated) at this time?
1. Aspirin
2. B blockers
3. Nitroglycerin
4. Tissue plasminogen activator (t-PA)

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 84

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Morphine, nitroglycerin, aspirin, oxygen, and b blockers are often administered in the setting of an acute myocardial infarction (Nfl). The administration of thrombolytics have been shown to improve outcome in patients with acute MI who exhibit chest pain (for> 30 minutes and < 12 hours), ST elevation of at least 0.1 mm in two contiguous leads, or new left bundle branch block and no evidence of heart failure or hypotension. Although the patient meets the criteria for the administration of t-PA, the recent surgical procedure makes this option less appealing due to the associated bleeding risk. Additionally, aspirin is universally
recommended for the treatment of acute MI and would not be contraindicated approximately 48 hours after a simple
microdiscectomy. The use of ~ blockers in this patient is contraindicated because the patienfs pulse is less than SO
(Marino, pp. 304-305, 309- 310).

Question 85

Match the appropriate vasopressor with the
appropriate characteristics. Answers may be used once,
more than once, or not at all.

Inotropic agent of choice for treatment of acute severe
heart failure

A. Isoproterenol
B. Dopamine
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Answer 85

A. Isoproterenol
B. Dopamine
**C. Dobutamine **
D. Epinephrine
E. Norepinephrine
F. None of the above

Isoproterenol is a potent ~ agonist that results in prominent
increases in cardiac output and deCl’eases in diastolic blood
pressure (peripheral vasodilation, )’ Isoproterenol promotes both positive inotropic and chronotropic actions.
Dopamine primarily activates dopaminergic receptors in the
renal, mesenteric, and cerebral vasculature at low dosages,
augmenting flow to these regions. At high dosages, dopamine
acts primarily as a vasoconstrictor, activating peripheral
(J. receptors. Dobutamine is primarily a ~l agonist that is
the inotropic agent of choice in acute, severe systolic heart
failure. Epinephrine stimulates both (J. and ~ receptors. At
low dosages, epinephrine stimulates primarily ~ receptors;
at high dosages, (J. receptors are primarily stimulated. As
opposed to dopamine, however, epinephrine is a potent renal
vasoconstrictor, even at low dosages. Norepinephrine is an
226 Intensive Neurosurgery Board Review
Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Question 86

Match the appropriate vasopressor with the
appropriate characteristics. Answers may be used once,
more than once, or not at all.

Primarily a, receptor agonist for shock states
A. Isoproterenol
B. Dopamine
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Answer 86

A. Isoproterenol
B. Dopamine
C. Dobutamine
D. Epinephrine
**E. Norepinephrine **
F. None of the above

Isoproterenol is a potent ~ agonist that results in prominent
increases in cardiac output and deCl’eases in diastolic blood
pressure (peripheral vasodilation, )’ Isoproterenol promotes both positive inotropic and chronotropic actions.
Dopamine primarily activates dopaminergic receptors in the
renal, mesenteric, and cerebral vasculature at low dosages,
augmenting flow to these regions. At high dosages, dopamine
acts primarily as a vasoconstrictor, activating peripheral
(J. receptors. Dobutamine is primarily a ~l agonist that is
the inotropic agent of choice in acute, severe systolic heart
failure. Epinephrine stimulates both (J. and ~ receptors. At
low dosages, epinephrine stimulates primarily ~ receptors;
at high dosages, (J. receptors are primarily stimulated. As
opposed to dopamine, however, epinephrine is a potent renal
vasoconstrictor, even at low dosages. Norepinephrine is an
226 Intensive Neurosurgery Board Review
Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Question 87

Match the appropriate vasopressor with the
appropriate characteristics. Answers may be used once,
more than once, or not at all.

Augments cerebral blood flow at low doses
A. Isoproterenol
B. Dopamine
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Answer 87

A. Isoproterenol
**B. Dopamine **
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Isoproterenol is a potent ~ agonist that results in prominent
increases in cardiac output and deCl’eases in diastolic blood
pressure (peripheral vasodilation, )’ Isoproterenol promotes both positive inotropic and chronotropic actions.
Dopamine primarily activates dopaminergic receptors in the
renal, mesenteric, and cerebral vasculature at low dosages,
augmenting flow to these regions. At high dosages, dopamine
acts primarily as a vasoconstrictor, activating peripheral
(J. receptors. Dobutamine is primarily a ~l agonist that is
the inotropic agent of choice in acute, severe systolic heart
failure. Epinephrine stimulates both (J. and ~ receptors. At
low dosages, epinephrine stimulates primarily ~ receptors;
at high dosages, (J. receptors are primarily stimulated. As
opposed to dopamine, however, epinephrine is a potent renal
vasoconstrictor, even at low dosages. Norepinephrine is an
226 Intensive Neurosurgery Board Review
Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Question 88

Match the appropriate vasopressor with the
appropriate characteristics. Answers may be used once,
more than once, or not at all.

Mainly 0,1 activity
A. Isoproterenol
B. Dopamine
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Answer 88

A. Isoproterenol
B. Dopamine
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Isoproterenol is a potent ~ agonist that results in prominent
increases in cardiac output and deCl’eases in diastolic blood
pressure (peripheral vasodilation, )’ Isoproterenol promotes both positive inotropic and chronotropic actions.
Dopamine primarily activates dopaminergic receptors in the
renal, mesenteric, and cerebral vasculature at low dosages,
augmenting flow to these regions. At high dosages, dopamine
acts primarily as a vasoconstrictor, activating peripheral
(J. receptors. Dobutamine is primarily a ~l agonist that is
the inotropic agent of choice in acute, severe systolic heart
failure. Epinephrine stimulates both (J. and ~ receptors. At
low dosages, epinephrine stimulates primarily ~ receptors;
at high dosages, (J. receptors are primarily stimulated. As
opposed to dopamine, however, epinephrine is a potent renal
vasoconstrictor, even at low dosages. Norepinephrine is an
226 Intensive Neurosurgery Board Review
Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Question 89

Match the appropriate vasopressor with the
appropriate characteristics. Answers may be used once,
more than once, or not at all.

Primarily B receptor agonist that increases cardiac
output and decreases diastolic blood pressure
A. Isoproterenol
B. Dopamine
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Answer 89

**A. Isoproterenol **
B. Dopamine
C. Dobutamine
D. Epinephrine
E. Norepinephrine
F. None of the above

Isoproterenol is a potent ~ agonist that results in prominent
increases in cardiac output and deCl’eases in diastolic blood
pressure (peripheral vasodilation, )’ Isoproterenol promotes both positive inotropic and chronotropic actions.
Dopamine primarily activates dopaminergic receptors in the
renal, mesenteric, and cerebral vasculature at low dosages,
augmenting flow to these regions. At high dosages, dopamine
acts primarily as a vasoconstrictor, activating peripheral
(J. receptors. Dobutamine is primarily a ~l agonist that is
the inotropic agent of choice in acute, severe systolic heart
failure. Epinephrine stimulates both (J. and ~ receptors. At
low dosages, epinephrine stimulates primarily ~ receptors;
at high dosages, (J. receptors are primarily stimulated. As
opposed to dopamine, however, epinephrine is a potent renal
vasoconstrictor, even at low dosages. Norepinephrine is an
226 Intensive Neurosurgery Board Review
Ct.-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Marino, pp. 281-286, 295- 296).

Question 90

A 62-year-old male is admitted to the ICU for the acute
management of severe hypertension after subendocardial
myocardi al infarction. The patient’s hypertension is refractory to intravenous labetalol, hydralazine, and nitroglycerin ,
however, it responds well to continuous nitroprusside infusion. The patient is then initiated on oral antihypertensive
therapies. The following day the patient experiences the
acute onset of confusion, tinnitus, nausea, tachycardia ,
abdominal pain, and blurred vision. What is the most appropriate next course of action ?
A. Obtain an arterial blood gas
B. Obtain a serum sodium level
C. Administration of IV lorazepam
D. Administration of IV methylene blue
E. Administration of IV hematin

Answer 90

A. Obtain an arterial blood gas
B. Obtain a serum sodium level
C. Administration of IV lorazepam
**D. Administration of IV methylene blue **
E. Administration of IV hematin

Prolonged nitroprusside infusions are associated with
the accumulation of cyanide, which grad ually exhausts
thiosulfate and methemoglobin reserves and can result in
cyanide toxicity. Cyanide accumulation can result in delirium, ataxia, tinnitus, abdominal pain, blurry vision, muscle
spasms, nausea, emesis, and dyspnea. \Vithout treatment,
cyanide toxicity can progress to metabolic acidosis, hypotension, coma , and death. Treatment of nitroprusside-induced
cyanide toxicity includes cessation of the medication and
IV methylene blue. Sodium nitrite , sodium thiosulfate , and
hemodialysis are also effective therapies (Marino, pp. 838-
841).

Question 91

Which of the following are useful in the treatment of
SIADI-I?
1. Fluid restriction
2. 3% sa line infusion
3. Demeclocycline
4. Hemodialysis

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

Answer 91

A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above

First-line therapy for asymptomatic patients with
hyponatremia secondary to SIADI-I entails fluid restriction.
The treatment of severe, symptomatic hyponatremia (typically Na < 120 mEq/L) secondary to SIADI-I involves more
aggressive correction with 3% saline infusions, which are
generally discontinued when the patient’s symptoms resolve
or the serum sodium reaches 128 to 130 mEq/L. The treatment of chronic SIADH often involves demeclocycline; the
treatment of SIADH in association with congestive heart failure or renal fail ure often involves hemodialysis (Greenberg,
pp.17- 19;Marino,p.643).

Question 92

What is the free water deficit of an 80 kg male (lean body
mass) with a serum sodium level of 148 mEq/L?

A. l.4 L
B. 2.7 L
C. 3.5 L
D. 4.8 L
E. 6.0 L

Answer 92

A. l.4 L
**B. 2.7 L **
C. 3.5 L
D. 4.8 L
E. 6.0 L

To calculate free water deficit, total body water
(TEW) must be calculated initially. TEW is 0.5 times lean
body mass (in kilograms) for a female and 0.6 times lean
body mass for a male. Free water deficit is then calculated by
multiplying TEW by (S1’,,-140)/140. Thus, the free water
deficit in this patient is 2.7 L (Greenberg, p. 19).

Question 93

Which of the following is a necessary cofactor in the
synthesis of collagen?
A. Vitamin D
B. Thiamine
C. Vitamin B12
D. Vitamin C
E. Pyridoxine

Answer 93

A. Vitamin D
B. Thiamine
C. Vitamin B12
**D. Vitamin C **
E. Pyridoxine

Vitamin C is a necessary cofactor in the synthesis of
collagen. Vitamin C is important in the intracellular hydroxylation of proline and lysine residues in the procollagen
molecule (Robbins, pp. 456- 459; Wilkins, pp. 519-520).

Question 94

Acute toxicity of which of the following vitamins can result
in headache , blurry vision, nausea, emesis, and papilledema
(elevated intracranial pressure) ?
A. Vitamin A
B. Vital’llin D
C. Vitamin E
D. Thiamine
E. Folate

Answer 94

**A. Vitamin A **
B. Vital’llin D
C. Vitamin E
D. Thiamine
E. Folate

Acute vitamin A toxicity can result in symptoms of
elevated intracranial pressure (headache, nausea, emesis,
blurry vision, papilledema), hepatomegaly, and ascites.
These symptoms are usually transient and typically resolve
after discontinuing the excessive intake of vitamin A; however, severely symptomatic patients occasionally require
serial lumbar punctures (to treat the elevated intracranial
pressure) and restoration of any underlying electrolyte
abnormalities (e.g. , hypercalcemia) (Robbins, p. 441).

Question 95

Which of the following characteristics is NOT typically
observed with Cushing’s syndrome?
A. J’I’Iuscle wealmess
B. Plethora
C. Loss of diurnal rhythm of cortisol secretion
D. High serum ACTI-I level
E. Solitary adrenal adenoma

Answer 95

A. J’I’Iuscle wealmess
B. Plethora
C. Loss of diurnal rhythm of cortisol secretion
**D. High serum ACTI-I level **
E. Solitary adrenal adenoma

Cushing’s syndrome usually results from iatrogenic
steroid administration or adrena l adenomas. Under these
circumstances, the diurnal rhythm of cortisol secretion is
lost and serul11 ACTH levels are markedly depressed. Rarely,
ectopic ACTH production by a malignant tumor occurs (e.g.,
oat cell carcinoma of the lung); tills can result in Cushing’s
syndrome with concomitant high serum ACTH levels.
Cushing’s disease results from an ACTH-producing pituitary
adenoma. The clinical symptomatology of Cushing’s syndrome and Cushing’s disease is similar and consist of truncal
obeSity, abdominal striae, acne, muscle weakness, hirsuitism, depression, lethargy, “moon faCies,” and plethora
(Greenberg, pp. 420-421).

Question 96

Match the following arterial blood gas values
with the appropriate acid/base disorder. Letters may be used
once, more than once, or not at all.

pH 7.27, PaC02 52 nllllI-Ig, I-ICO:; 23 I11Eq/L
A. Respiratory acidosis
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

Answer 96

**A. Respiratory acidosis **
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

The normal range for pH is 7.36
to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to
26 mEq/L. The initial step in the interpretation of acid-base
disorders involves determining whether the disorder is
primarily respiratory or metabolic. With primary metabolic
acid-base disorders, the changes in pH and PC02 occur in
the same direction. \Vith primary respiratory disorders, the
changes in pH and PC02 occur in opposite directions. The
absolute value of the PC02 and the change in the pH are then
used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected
compensatory change in PC02 for metabolic acidosis is 1.5
I-ICOJ + (8 ± 2). The expected compensatory change in PC02
for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is
normal, higher (respiratory acidosis) or lower (respiratory
alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can
be calculated to determine whether a metabolic acid-base
disorder is also present. With acute respiratory acidosis, the
expected change in pH is 0.008 X (PC02 - 40). With acute
respiratory alkalosis, the expected change in pH is 0.008 x
(40 - PC02). If the change in pH exceeds 0.008 times the
change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated)
respiratory disorders, the change in pH is 0.003 times the
change in PC02 . In question 96, the values are consistent
with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial
respiratory compensation. Question 98 is fully compensated
respiratory acidosis. Question 99 is metabolic acidosis with
partial respiratory compensation. Question 100 is combined
respiratory and metabolic acidosis (Marino, pp. 581- 586).

Question 97

Match the following arterial blood gas values
with the appropriate acid/base disorder. Letters may be used
once, more than once, or not at all.

pI-I 7.48, PaC02 45 I11mI-Ig, I-ICO:; 32 I11Eq/L
A. Respiratory acidosis
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

Answer 97

A. Respiratory acidosis
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
**D. Metabolic alkalosis **
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

The normal range for pH is 7.36
to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to
26 mEq/L. The initial step in the interpretation of acid-base
disorders involves determining whether the disorder is
primarily respiratory or metabolic. With primary metabolic
acid-base disorders, the changes in pH and PC02 occur in
the same direction. \Vith primary respiratory disorders, the
changes in pH and PC02 occur in opposite directions. The
absolute value of the PC02 and the change in the pH are then
used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected
compensatory change in PC02 for metabolic acidosis is 1.5
I-ICOJ + (8 ± 2). The expected compensatory change in PC02
for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is
normal, higher (respiratory acidosis) or lower (respiratory
alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can
be calculated to determine whether a metabolic acid-base
disorder is also present. With acute respiratory acidosis, the
expected change in pH is 0.008 X (PC02 - 40). With acute
respiratory alkalosis, the expected change in pH is 0.008 x
(40 - PC02). If the change in pH exceeds 0.008 times the
change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated)
respiratory disorders, the change in pH is 0.003 times the
change in PC02 . In question 96, the values are consistent
with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial
respiratory compensation. Question 98 is fully compensated
respiratory acidosis. Question 99 is metabolic acidosis with
partial respiratory compensation. Question 100 is combined
respiratory and metabolic acidosis (Marino, pp. 581- 586).

Question 98

Match the following arterial blood gas values
with the appropriate acid/base disorder. Letters may be used
once, more than once, or not at all.

pI-I 7.35, PaC02 48 I11mHg, I-ICO:; 28 mEq/L
A. Respiratory acidosis
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

Answer 98

**A. Respiratory acidosis **
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

The normal range for pH is 7.36
to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to
26 mEq/L. The initial step in the interpretation of acid-base
disorders involves determining whether the disorder is
primarily respiratory or metabolic. With primary metabolic
acid-base disorders, the changes in pH and PC02 occur in
the same direction. \Vith primary respiratory disorders, the
changes in pH and PC02 occur in opposite directions. The
absolute value of the PC02 and the change in the pH are then
used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected
compensatory change in PC02 for metabolic acidosis is 1.5
I-ICOJ + (8 ± 2). The expected compensatory change in PC02
for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is
normal, higher (respiratory acidosis) or lower (respiratory
alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can
be calculated to determine whether a metabolic acid-base
disorder is also present. With acute respiratory acidosis, the
expected change in pH is 0.008 X (PC02 - 40). With acute
respiratory alkalosis, the expected change in pH is 0.008 x
(40 - PC02). If the change in pH exceeds 0.008 times the
change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated)
respiratory disorders, the change in pH is 0.003 times the
change in PC02 . In question 96, the values are consistent
with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial
respiratory compensation. Question 98 is fully compensated
respiratory acidosis. Question 99 is metabolic acidosis with
partial respiratory compensation. Question 100 is combined
respiratory and metabolic acidosis (Marino, pp. 581- 586).

Question 99

Match the following arterial blood gas values
with the appropriate acid/base disorder. Letters may be used
once, more than once, or not at all.

pH 7.31 , PaC02 34 I11mI-Ig, IlCO:; 19 mEq/L
A. Respiratory acidosis
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

Answer 99

A. Respiratory acidosis
B. Respiratory alkalosis
**C. J’I’Ietabolic acidosis **
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

The normal range for pH is 7.36
to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to
26 mEq/L. The initial step in the interpretation of acid-base
disorders involves determining whether the disorder is
primarily respiratory or metabolic. With primary metabolic
acid-base disorders, the changes in pH and PC02 occur in
the same direction. \Vith primary respiratory disorders, the
changes in pH and PC02 occur in opposite directions. The
absolute value of the PC02 and the change in the pH are then
used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected
compensatory change in PC02 for metabolic acidosis is 1.5
I-ICOJ + (8 ± 2). The expected compensatory change in PC02
for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is
normal, higher (respiratory acidosis) or lower (respiratory
alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can
be calculated to determine whether a metabolic acid-base
disorder is also present. With acute respiratory acidosis, the
expected change in pH is 0.008 X (PC02 - 40). With acute
respiratory alkalosis, the expected change in pH is 0.008 x
(40 - PC02). If the change in pH exceeds 0.008 times the
change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated)
respiratory disorders, the change in pH is 0.003 times the
change in PC02 . In question 96, the values are consistent
with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial
respiratory compensation. Question 98 is fully compensated
respiratory acidosis. Question 99 is metabolic acidosis with
partial respiratory compensation. Question 100 is combined
respiratory and metabolic acidosis (Marino, pp. 581- 586).

Question 100

Match the following arterial blood gas values
with the appropriate acid/base disorder. Letters may be used
once, more than once, or not at all.

pH 7.28, PaC02 40 nlluI-Ig, I-ICO:; 19 mEq/L
A. Respiratory acidosis
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
E. Combined respiratory acidosis and metabolic acidosis
F. Combined respiratory alkalosis and metabolic alkalosis

Answer 100

A. Respiratory acidosis
B. Respiratory alkalosis
C. J’I’Ietabolic acidosis
D. Metabolic alkalosis
**E. Combined respiratory acidosis and metabolic acidosis **
F. Combined respiratory alkalosis and metabolic alkalosis

The normal range for pH is 7.36
to 7.44; for PC02 36 to 44 111111 I-Ig; and for HCO.) 22 to
26 mEq/L. The initial step in the interpretation of acid-base
disorders involves determining whether the disorder is
primarily respiratory or metabolic. With primary metabolic
acid-base disorders, the changes in pH and PC02 occur in
the same direction. \Vith primary respiratory disorders, the
changes in pH and PC02 occur in opposite directions. The
absolute value of the PC02 and the change in the pH are then
used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as well. The expected
compensatory change in PC02 for metabolic acidosis is 1.5
I-ICOJ + (8 ± 2). The expected compensatory change in PC02
for metabolic alkalosis is 0.7 HCOJ + (21 ± 2). If the PC02 is
normal, higher (respiratory acidosis) or lower (respiratory
alkalosis) than the expected value , a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in pH can
be calculated to determine whether a metabolic acid-base
disorder is also present. With acute respiratory acidosis, the
expected change in pH is 0.008 X (PC02 - 40). With acute
respiratory alkalosis, the expected change in pH is 0.008 x
(40 - PC02). If the change in pH exceeds 0.008 times the
change in PC02 , a superimposed metabolic acid-base disorder exists. In addition, with chronic (fully compensated)
respiratory disorders, the change in pH is 0.003 times the
change in PC02 . In question 96, the values are consistent
with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial
respiratory compensation. Question 98 is fully compensated
respiratory acidosis. Question 99 is metabolic acidosis with
partial respiratory compensation. Question 100 is combined
respiratory and metabolic acidosis (Marino, pp. 581- 586).