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2011 BRS2

Board Review Session II
Wednesday, August 17, 2011
Questions and Answers and Rationales

15. A patient is receiving volume assist-control ventilation and his ventilator graphics are
depicted as “Baseline” in the Figure. The top tracing in the Figure is flow, the second
tracing is volume, the third tracing is airway pressure, and the bottom tracing is
esophageal pressure. An aspiration event producing parenchymal lung injury occurs.
Which set of tracings is most consistent with this?

a. Panel A
b. Panel B
c. Panel C
d. Panel D

16. Curve A is the intraoperative capnograph of a 67-year-old man who underwent left
carotid endarterectomy 6 hours ago. He has diabetes and hypercholesterolemia. Findings
of preoperative pulmonary assessment, including full pulmonary function tests, are
normal. Evaluation is requested for sudden hypotension and chest pain. There is no
change in pulse oximetry readings or lung auscultation.
Which of the following capnographs most suggests acute myocardial infarction as a cause

for this patient's symptoms?

a. Capnograph A
b. Capnograph B
c. Capnograph C
d. Capnograph D

17. A man with an exacerbation of chronic obstructive pulmonary disease has required
mechanical ventilatory support for the past 5 days. This morning, his gas exchange has
improved, his airway obstruction seems less, and he is easily triggering every breath on
the ventilator. A spontaneous breathing trial (SBT) is initiated and, although he does well
initially, he becomes tachypneic and tachycardic, and his SpO2 drops after 1 hour.
The best way to manage this patient's ventilatory support is to:
a. Abandon further SBTs, place him on substantial pressure support (PS) ventilation and
wean the pressure level as tolerated
b. Abandon further SBTs, start a combination of synchronized intermittent mandatory
ventilation (SIMV) and PS, then sequentially wean the SIMV and PS as tolerated.
c. Repeat the SBTs every 6 hours and provide stable PS ventilation in between.
d. Repeat the SBTs every 24 hours and provide stable PS ventilation in between.
e. Repeat the SBTs every 24 hours and suppress all spontaneous efforts in between.

18. A 34-year-old woman is receiving mechanical ventilation for bilateral lung
contusions. She is receiving volume assist-control ventilation (tidal volume, 6 mL/kg
ideal body weight; plateau pressure, 23 cm H2O; positive end-expiratory pressure, 5 cm
H2O; FIO2, 0.40; SpO2, 93%) and has been heavily sedated for over 72 hours. As a
consequence, she never triggers the ventilator and relies on the ventilator set rate. Under
these circumstances, she is particularly at risk for:

a. Intracranial hypertension
b. Oxygen toxicity
c. Ventilator-induced diaphragmatic dysfunction
d. Pneumothorax
19. A patient is being ventilated with the mode depicted in the Figure below (top tracings
depict flow; middle tracings, volume; bottom tracings, pressure). The left panel is a stable
baseline. Flash pulmonary edema develops and the graphics change to the right panel.
Which of the following ventilation modes behaves like this?
a. Pressure-regulated volume control ventilation
b. Pressure support ventilation

c. Volume assist-control ventilation
d. Airway pressure release ventilation

Figure A

Figure B

20. In cardiogenic shock following myocardial infarction, which of the following
therapies will produce all of the following hemodynamic and myocardial effects: an
increase in mean arterial pressure, a decrease in systemic vascular resistance (afterload),
an increase in myocardial oxygen supply (coronary blood flow), and a decrease in
myocardial oxygen demand?
a. Norepinephrine
b. Milrinone
c. Dobutamine
d. Intraaortic balloon counterpulsation
21. A 48-year-old man enters the ICU with a 2-hour history of severe (10/10), substernal,
nonradiating chest pain. He notes some pain reduction with leaning forward. He has mild

nausea but not shortness of breath or diaphoresis. His father had a myocardial infarction
at the age of 49. He takes no medications and has no other past medical history. His pulse
rate is 82/min, BP is 160/90 mm Hg, temperature is 38.2°C (100.8°F), and RR is 18/min.
His physical examination findings are normal. His ECG is shown in the Figure below. A
cardiac catheterization laboratory is not available.
Which of the following therapeutic agents should be administered to this patient?

a. Tenecteplase (TNK-tPA)
b. Ibuprofen
c. Abciximab
d. Heparin

22. A 72-year-old woman enters the ICU with an acute inferior myocardial infarction and
bradycardia at 56/min. She has a past history of atrial fibrillation and has received longterm warfarin therapy. She is treated with tenecteplase (TNK-tPA), heparin, aspirin, and
captopril. Beta-blockers are held due to her bradycardia, and a temporary transvenous
pacemaker is fluoroscopically positioned in the right ventricular apex with good sensing
and pacing thresholds. The patient’s chest pain resolves about 30 minutes after
tenecteplase administration.
The patient’s ECG on the second hospital day is shown in the Figure below.
In addition to an evolving inferoposterior myocardial infarction, the ECG shows which of
the following?

a. Dual-chamber pacing
b. Failure to capture only
c. Failure to sense only
d. Failure to sense and capture
e. Rate-adaptive pacing

23. A patient with recent acute inferior myocardial infarction awaiting coronary artery
bypass grafting develops recurrent chest pain and becomes unresponsive and pulseless
during ECG. His ECG is shown in the Figure below. The patient has an IV line in place
and receives direct electrical defibrillations, but he remains in the rhythm shown in the
ECG. Cardiopulmonary resuscitation is continued with chest compressions and
endotracheal intubation and ventilation.
Which of the following is the most appropriate next management step?

d.Intraaortic balloon pump
e.Immediate coronary artery bypass grafting

24. A 45-year-old woman with recently diagnosed small cell lung cancer is admitted 12
hours after her first dose of chemotherapy with altered mental status and oliguria. Her BP
is 95/60 mm Hg, HR is 88/min, and temperature is 37.3°C (99.1°F). Physical
examination is remarkable for confusion and tetany. Her urinalysis shows needle-shaped
The patient’s condition is associated with:
a. Hypouricemia
b. Hypercalcemia
c. Low lactate dehydrogenase level
d. High creatine kinase level

25. A 68-year-old woman with a history of depression and hyperlipidemia presents with
onset of confusion and lethargy during the past 24 hours. Medications include sertraline
and simvastatin. On examination, she is difficult to arouse and disoriented to time and

place. BP is 130/78 mm Hg, HR is 88/min, and she is afebrile. Her jugular venous
pressure is 6 cm at 45°. Lungs are clear. She has no edema. She is noncooperative with
neurologic examination, though no obvious focal findings are evident. Laboratory
findings in serum include the following: sodium, 114 mEq/L; potassium, 3.8 mEq/L;
blood urea nitrogen, 15 mg/dL; creatinine, 0.9 mg/dL; and glucose, 98 mg/dL. Urine
sodium level is 48 mEq/L, with osmolality of 450 mOsm/kg H2O.
Which of the following is the most appropriate first step in the management of her
a.Fluid restriction and observation with the goal of raising serum sodium level to 124
mEq/L in 24 hours
b. IV 0.9% saline with the goal of raising her serum sodium level to 124 mEq/L in 24
c. IV 0.9% saline and furosemide with the goal of raising her serum sodium level to 130
mEq/L in 24 hours
d. IV 3% saline with the goal of rapidly raising her serum sodium level to 118 mEq/L in
4 hours

26. An intensivist is called to a resuscitation of an elderly patient with a small bowel
obstruction. The patient has vomitus coming out of her mouth and is hemodynamically
unstable, with a systolic BP of 75 mm Hg. She is oxygenating on a face mask but is
poorly responsive. Etomidate and 1.0 mg/kg of rocuronium are given and cricoid pressure
is being held. Endotracheal intubation is attempted twice but the view is very poor. The
patient is becoming more hypotensive and hypoxemic.
Which of the following would be most useful in the next attempt at establishing an
a. Using another laryngoscopy blade
b. Using a laryngeal mask airway
c. Using a cricothyroidotomy kit
d. Doing a blind nasal intubation
e. Getting a smaller endotracheal tube
27. A 51-year-old woman with exertional angina is admitted to the ICU after having a
cardiac arrest during an exercise test. Her prior medical history includes coronary artery
disease treated with coronary artery bypass grafting 8 months ago, hypertension,
hyperlipidemia, and diabetes. She currently takes extended-release metoprolol, 50
mg/day; ramipril, 2.5 mg/day; simvastatin, 80 mg day; aspirin, 81 mg/day; metformin,
500 mg 3 times daily; and repaglinide, 2 mg 3 times daily. During the recovery phase of
the exercise test, the patient collapsed and the ECG shown in the Figure was obtained.
The ECG shows which of the following rhythms?

Comment [A1]: ECG missing

a. Atrial fibrillation with a bundle-branch block
b. Wolff-Parkinson-White syndrome
c. Ventricular fibrillation
d. Ventricular tachycardia
28. A 52-year-old woman with dilated cardiomyopathy and heart failure enters the ICU
because of increasing dyspnea and weight gain during the past week. An arterial and
pulmonary artery catheter are placed. Baseline and postmedication hemodynamics are
shown below.
Following Drug
Blood pressure (mm Hg)
Right atrial pressure (mean, mm Hg)
Right ventricular pressure (mm Hg)
Pulmonary artery pressure (mm Hg)
Pulmonary artery occlusion
Pressure (mean, mm Hg)
Cardiac output (L/min)
Urine output (mL/h)
The hemodynamic change depicted in the table is most consistent with the administration
of which of the following medications?
a. Nesiritide
b. Dopamine
c. Norepinephrine
d. Angiotensin

e. Hydralazine

29. A 74-year-old man enters the ICU with fever and hypotension. He has a history of
kidney stones with multiple previous bouts of urinary tract infection. Urine and blood
cultures are obtained, and vancomycin and ceftazidime are started. Presently, his BP is
70/40 mm Hg. Two liters of normal saline do not raise the blood pressure, and a
thermodilution pulmonary artery catheter is inserted, revealing low right-sided heart
filling pressures, a pulmonary artery occlusion pressure of 16 mm Hg, and a cardiac
output of 13.7 L/min. An infusion of norepinephrine increases the blood pressure to
100/70 mm Hg. An infusion of vasopressin, 0.01–0.03 U/min, is also started.
Which of the following statements most accurately reflects the evidence on the
effectiveness of vasopressin, 0.01–0.03 U/min, as administered to this patient?
a. Patients on doses of norepinephrine >15 µg/min demonstrate an improved survival if
so treated.
b. When added to norepinephrine, it is associated with an increase in episodes of acute
ischemic heart disease.
c. Given with norepinephrine, it produces a mortality rate at 28 days that is comparable to
therapy with norepinephrine alone.
d. It has little or no effect on the ability to decrease norepinephrine dose using a target
mean arterial pressure of 65 to 75 mm Hg.

15. Correct Answer: B. Panel B
Rationale: Because the mode is volume assist-control, the set volume is constant
regardless of respiratory system mechanics in all four panels. In contrast, the airway and
the esophageal pressure profiles are markedly different. In all four choices, the peak
airway pressures are elevated, but only in B and C are the plateau pressures (pressures at
end-inspiration with no flow) elevated. Thus panels B and C are the only two patterns
reflecting a worsening respiratory system compliance, as would occur with a
parenchymal lung injury such as our patient experienced.
The esophageal pressure allows us to separate the lung and the chest wall compliance
contributions to the plateau pressure in panels B and C. If the elevation in plateau
pressure is due to a chest wall effect such as obesity, ascites, anasarca, or chest bandages,
the esophageal pressure will be elevated, as in panel C. However, if abnormal lung
mechanics are producing the acutely elevated plateau pressure, the esophageal pressure
will not change. Thus, panel B best represents an acute parenchymal lung injury, as in our
Panels A and D reflect flow-related pressure elevations, as might occur with increased
airway resistance (panel A) or an increased flow setting (panel D).
16. Correct Answer: B. Capnograph B
Rationale: Arterial end-tidal PaCO2 gradient is a function of dead-space ventilation, and
in the absence of significant pulmonary disease, end-tidal partial pressure of carbon
dioxide (PetCO2) is several millimeters of mercury less than the pressure of arterial
carbon dioxide (PaCO2). The major factors that alter this gradient are lung disease and
change in cardiac output. An acute change in the gradient without a significant change in
capnographic configuration indicates a change in cardiac output. In our case, curve A
represents the baseline capnograph; curve B shows a widened P(arterial to end-tidal [aet])CO2 gradient while the morphology of the capnograph is similar to the baseline curve,
suggesting an acute change in cardiac output as a cause for the patient's instability.
Curves C and D, although suggestive of a widened P(a-et)CO2 gradient show different
morphologies than curve A. This difference in morphology suggests, in addition, changes
in pulmonary mechanics as an explanation for the observed changes.
17. Correct Answer: D. Repeat the SBTs every 24 hours and provide stable PS
ventilation in between.
Rationale: The evidence strongly supports daily spontaneous breathing trials (SBTs) as
the best way to assess ventilator discontinuation potential in patients with stable or
recovering respiratory failure. Specifically, in two large trials evaluating ventilator
weaning and withdrawal techniques in such patients, no strategy was faster than simply
evaluating the patient daily with an SBT and maintaining a stable level of substantial
ventilatory support in between. Indeed, strategies focused only on gradual support
reductions without daily SBTs can actually slow the withdrawal process if support

reductions are not timely. Moreover, because gradual support reductions require a high
level of monitoring and frequent ventilator adjustments, personnel time and resource
consumption can be increased. Options A and B are thus wrong.
While more frequent SBTs (option C) may be useful in patients with rapidly reversible
respiratory failure (eg, drug overdose, asthma, transient need for neuromuscular blockers
for procedures), lung injury recovery patterns are such that SBTs more frequent than
every 24 hours are not helpful. Option C is thus wrong in this patient with chronic
obstructive pulmonary disease.
The difference between options D and E is the approach to the stable ventilatory support
between the daily SBTs. Animal studies have shown that muscle atrophy and delayed
fatigue recovery occurs when the inspiratory muscles are made totally inactive (option
E). Moreover, sedation needs may increase if the goal is to totally suppress all inspiratory
activity. Thus, the preferred ventilatory mode should probably be a comfortable
interactive mode such as pressure support (option D) with the inspiratory pressure level
titrated to comfort.
18. Correct Answer: C. Ventilator-induced diaphragmatic dysfunction
Rationale: Ventilator-induced diaphragmatic dysfunction (VIDD) describes ventilatory
muscle abnormalities induced by mechanical ventilation strategies that suppress or
eliminate spontaneous ventilatory muscle activity. These strategies generally involve
high-level assist-control support modes designed to have patients perform little or no
work to receive ventilatory support. Ventilatory muscles thus receive virtually no neural
stimulation and have virtually no muscle loading.
Under circumstances of no neural input or muscle loading, a number of changes have
been described in the ventilatory muscles that resemble peripheral skeletal muscle
atrophy. Complicating this is the fact that VIDD co-occurs with other causes of muscle
injury (eg, critical illness myopathy, corticosteroids, neuromuscular blockers) and it may
be difficult to clinically discern its relative importance. Nevertheless, it seems prudent to
avoid prolonged conventional mechanical ventilation and allow spontaneous inspiratory
efforts as soon as feasible with appropriate levels of mechanical ventilatory support.
While options A, B, and D may all be complications of mechanical ventilation, they are
not the best choices in the clinical setting described here. The patient's intrathoracic
pressures are not high enough to significantly raise intracranial pressures or produce
pneumothorax, her FIO2 is in a range that minimizes oxygen toxicity, and her lack of
inspiratory efforts makes dyssynchrony a nonissue.
19. Correct Answer: A. Pressure-regulated volume control ventilation
Rationale: The left panel of the figure depicts a pressure-targeted mode with the typical
square wave of pressure and the exponentially decelerating inspiratory flow pattern. With
abruptly changing respiratory system mechanics such as flash pulmonary edema,
traditional pressure-targeted modes (ie, pressure assist-control and pressure support) will

maintain the set airway pressure but produce smaller tidal volumes. That appears to be
the case in the first breath of the lower panel. However, over the next several breaths, the
ventilator automatically increases the inspiratory pressure to restore the previous tidal
volume. This is characteristic of the pressure-regulated volume control mode (option A).
The pressure-regulated volume control mode is designed to provide the synchrony and
gas mixing effects of pressure targeting while “guaranteeing” a set tidal volume. A
similar feedback algorithm can be applied to pressure support in the volume support
20. Correct Answer: D. Intra-aortic balloon counterpulsation
Rationale: The hemodynamic and myocardial effects of an increase in mean arterial
pressure and a decrease in systemic vascular resistance coupled with an increase in
myocardial oxygen supply (coronary blood flow) and a decrease in myocardial oxygen
demand are typical of effective treatment with intra-aortic balloon counterpulsation
(IABC). IABC provides a balloon inflation-induced augmentation of blood pressure and
flow during ventricular diastole. With effective IABC, the mean arterial pressure
increases because of the added balloon-assisted pressure wave during diastole. Overall,
stroke volume and cardiac output are increased, leading to a reduction in systemic
vascular resistance and afterload. The IABC also increases diastolic blood flow into the
coronary vessels, probably because of direct balloon inflation and an overall
improvement in hemodynamics from restoration of blood pressure and cardiac output.
This constellation of hemodynamic and myocardial effects is ideal for the management of
cardiogenic shock because it optimizes the systemic and cardiac circulations in the face
of major ventricular failure and shock.
No pharmacologic agent is able to produce these hemodynamic and myocardial effects.
Norepinephrine’s vasoconstrictor properties increase blood pressure and increase
systemic vascular resistance; norepinephrine increases myocardial oxygen demand
because of the increase in afterload, and myocardial oxygen supply usually increases as a
result of improvement in systemic blood pressure. Therefore, option A is incorrect.
Dobutamine and milrinone both decrease systemic vascular resistance by vasodilation
and increase cardiac output because of their inotropic actions; however, blood pressure
usually decreases, especially with milrinone, so options B and C are incorrect.
Dobutamine causes an increase in both myocardial oxygen demand and supply because
of its beta1-adrenergic inotropic stimulation. Myocardial oxygen consumption usually
increases with dobutamine. Milrinone has a somewhat more potent vasodilator effect than
dobutamine, so milrinone also increases myocardial oxygen supply and demand;
however, the increase is more balanced, so that myocardial oxygen consumption is
usually unchanged.
21. Correct Answer: B. Ibuprofen
Rationale: The patient’s chest pain improves somewhat on leaning forward, a
characteristic commonly seen in pericarditis. The ECG shows diffuse ST-segment
elevation located in the inferior (II, III, aVF), lateral (I, II, aVL), and most anterior (V3-

V6) leads. In addition, prominent PR depression is seen in leads II and aVF. Lead aVR
shows PR-segment elevation and ST-segment depression. These diffuse ECG changes are
typical of acute pericarditis, which should be treated with a nonsteroidal antiinflammatory agent (NSAID) such as ibuprofen. Option B is correct.
The typical features of ECG abnormalities in acute pericarditis are the diffuse ST
elevation commonly in all leads except aVR and V1 (as in this case) and PR-segment
depression in several leads. The PR-segment elevation and ST depression in aVR are also
typical of pericarditis. Treatment with an NSAID such as ibuprofen is usually effective.
In resistant cases, indomethacin, colchicine, and rarely prednisone, are necessary to
relieve symptoms.
Since this patient has pericarditis, none of the other agents aimed at the coagulation
system are indicated. Tenecteplase is a thrombolytic agent that would be indicated in
treatment of an ST-segment elevation myocardial infarction (MI), with ST elevation in
the leads corresponding to the occluded coronary artery. (Option A is incorrect.)
Abciximab is a platelet IIb/IIIa receptor antagonist that would be indicated in acute STsegment elevation MI being treated with primary angioplasty. (Option C is incorrect.)
Heparin is an antithrombin agent that should be used with tenecteplase, reteplase, or
alteplase for reperfusion therapy during an ST-segment elevation MI. (Option D is
In patients with more equivocal ECG findings, an echocardiogram may provide useful
information to differentiate pericarditis from an ST-elevation MI. A patient with MI
should have obvious wall motion abnormalities, and a patient with pericarditis may have
some pericardial effusion. Elevation of troponin level may be seen in a minority of
patients with pericarditis, presumably reflecting some asymptomatic myocarditis
occurring with pericarditis. The troponin elevations are usually small and do not
approach the magnitude seen with MI.
22. Correct Answer: D. Failure to sense and capture
Rationale: The ECG shows atrial fibrillation with a moderate ventricular response and an
evolving inferior myocardial infarction (Qs and ST elevation in leads II, III, and aVF)
and posterior involvement (prominent R waves in V2 and V3 with ST depression in V2).
The pacemaker artifacts (arrows) march through the entire tracing at a rate of 60/min,
demonstrating that the pacemaker fails to sense the native rhythm. Pacemaker artifact
numbers 1, 5, and 7 occur far enough outside the refractory period of the ventricle that
they should produce capture if the pacemaker was capturing the ventricle. In this patient,
the ventricular pacemaker wire had dislodged into the pulmonary artery outflow tract and
was no longer sensing or capturing.
Dual-chamber pacing refers to pacing both the atrium and ventricle with separate pacing
wires. An atrial pacing wire was not placed in this patient, and atrial pacing would not be
successful in atrial fibrillation. Rate-adaptive pacing refers to permanent pacemakers that

have special programming features that increase heart rate in response to hemodynamic
or respiratory parameters. This form of permanent pacing was not used in this patient.
23. Correct Answer: B. Epinephrine
Rationale: The patient developed ventricular fibrillation (VF) during the performance of
an ECG for chest pain, probably ischemic in origin. Although the VF has a sinusoidal
pattern suggestive of torsade de pointes, the patient has become unresponsive and
pulseless, so this must be managed as a VF-induced sudden death. According to the
American Heart Association’s recommendations, IV epinephrine injection, 1 mg repeated
every 3-5 minutes, is the appropriate next step. An alternative to epinephrine (not a
choice in this question) would be IV vasopressin, 40 units. The American Heart
Association’s algorithm then recommends one minute of CPR and repeat electrical
defibrillation with 360 J.
Since epinephrine or vasopressin are the next steps in the accepted algorithm, the other
answers are incorrect. Atropine may be useful in treating bradycardia, symptomatic heart
block, asystole, or occasionally pulseless electrical activity with a slow rhythm. Calcium
may be useful in managing hyperkalemia and hypocalcemia. An intra-aortic balloon
pump would not be able to support the circulation of a patient with VF. An intra-aortic
balloon pump needs a rhythm or an arterial waveform in order to assist the circulation.
One needs to establish a rhythm and blood pressure in this patient before sending him for
coronary artery bypass grafting.
Insertion of a biventricular assist device (not a choice in this question) to fully take over
cardiac function as a possible bridge to coronary artery bypass grafting has been
described in a few reports of prolonged, unresponsive CPR.
24. Correct Answer: A. Hypouricemia
Rationale: Tumor lysis syndrome (TLS) is observed after chemotherapy for rapidly
growing tumors such as Burkitt lymphoma and leukemia. Recently, TLS has been
observed in patients with solid tumors such as small cell lung cancer, metastatic lung
cancer, and medulloblastoma. Hyperuricemia, hyperkalemia, hyperphosphatemia, and
hypocalcemia can appear as soon as 6 hours after chemotherapy and persist for 5 to 7
days after treatment. Serum calcium levels drop from ectopic calcium deposition; this
becomes more likely as the calcium-phosphorus product increases. Needle-shaped urate
crystals can form in the renal collecting ducts and result in oliguric and anuric renal
failure. High creatine kinase level is a typical finding of rhabdomyolysis, not TLS.
25. Correct Answer: D. IV 3% saline with the goal of rapidly raising her serum sodium
level to 118 mEq/L in 4 hours
Rationale: This patient has the syndrome of inappropriate antidiuresis, probably because
of sertraline. She presents with advanced neurologic complications of hyponatremia.
Regardless of the duration of the hyponatremia, such symptoms demand prompt

treatment to avoid further complications from hyponatremic encephalopathy due to
cerebral edema. Hypertonic saline is the treatment of choice, with the goal of increasing
the serum sodium level by 2-4 mEq/L over a period of 2-4 hours. After this modest
improvement, which is safe and advisable, then the patient should receive, in addition to
fluid restriction, either more hypertonic saline or the combination of normal saline and
furosemide while monitored every 2 hours. The goal is to correct her sodium level by no
more than 12 mEq/L in the first 24 hours, and by no more than 18 mEq/L in 48 hours.
Fluid restriction alone is not an acceptable treatment for symptomatic patients. Normal
saline, with or without furosemide, has limited effect in euvolemic patients and should
not be used in patients with severe symptoms.
26. Correct Answer: C. Using a cricothyroidotomy kit
Rationale: The patient is becoming unstable and could arrest. Furthermore, she is
paralyzed, so a blind nasal intubation cannot be done. Data has suggested that after two
attempts, consideration of obtaining a surgical airway is appropriate in critically ill
patients to prevent cardiac arrests. Furthermore, placement of a laryngeal mask airway
will not protect against aspiration in a patient who clearly is at risk. Continuing to
perform laryngoscopy is dangerous, unless a specific issue could be resolved with new
equipment. Using a smaller endotracheal tube will not help if you cannot visualize the
27. Correct Answer: C. Ventricular fibrillation
Rationale: The ECG shows coarse ventricular fibrillation. The patient was successfully
defibrillated. Cardiac catheterization showed a total occlusion of the bypass graft to the
obtuse marginal branch of the left circumflex coronary artery. Successful angioplasty and
stenting of the native left circumflex coronary artery was performed. The ventricular
fibrillation was probably the result of acute ischemia from the occluded bypass graft.
28. Correct Answer: A. Nesiritide
Rationale: The hemodynamic effect was a mild decrease in blood pressure, moderate
decrease in pulmonary and right heart pressures, and an increase in cardiac and urine
output. Nesiritide is the only agent listed that could produce this hemodynamic profile.
Nesiritide is a recombinant form of human B-type natriuretic peptide (BNP), which is a
naturally occurring protein secreted by the heart as part of the response to acute heart
failure. Nesiritide is a 32-amino-acid polypeptide that is synthesized using recombinant
DNA technology. BNP is expressed by ventricular myocytes in response to pressurevolume overloading of the ventricles. It has vasodilating and natriuretic properties that
counter the vasoconstricting and fluid retention effects of the renin-angiotensin system.
Nesiritide binds to the natriuretic peptide receptor on the surface of vascular smooth
muscle and endothelial cells and produces vasodilatation through a guanosine
monophosphate pathway.

When given to patients with heart failure, nesiritide reduces pulmonary artery occlusion
pressure, pulmonary artery pressure, right atrial pressure, and systemic vascular
resistance (SVR). Reduced SVR results in increased cardiac output. Thus, the agent
produces a “balanced” vasodilator effect on the pulmonary and systemic vascular circuits.
Nesiritide also produces a modest natriuretic and diuretic effect, and its hemodynamic
effects will enhance the effect of loop diuretics. The drug elimination half-life is about 20
minutes, and all effect is gone 2 to 4 hours after discontinuation of infusion. It was
approved by the FDA for treatment of acute heart failure in 2001.
Of the other choices, dopamine, norepinephrine, and angiotensin would produce an
increase in blood pressure and no change or an increase in pulmonary artery and
pulmonary artery occlusion pressures. Hydralazine is a pure arteriolar vasodilator. It will
produce a decrease in SVR and increase in cardiac output, but it will not produce a
decrease in pulmonary artery or pulmonary artery occlusion pressures.
29. Correct Answer: C. Given with norepinephrine, it produces a mortality rate at 28
days that is comparable to therapy with norepinephrine alone.
Rationale: A recently published, large, randomized, controlled trial, the Vasopressin in
Septic Shock Trial (VASST) compared therapy using vasopressin plus norepinephrine to
norepinephrine alone in 778 patients with septic shock. The study’s major finding was
that, in septic shock treated with catecholamine vasopressors, low-dose vasopressin
(0.01–0.03 U/min) did not reduce mortality compared to norepinephrine. Thus, option C
is correct.
VASST identified two prospectively defined subgroups of more severe septic shock,
patients requiring at least 15 µg/min of norepinephrine, and less severe septic shock,
those patients requiring <15 µg/min of norepinephrine. In the more severe septic shock
group, there was no difference in the mortality rates between vasopressin and
norepinephrine treatment groups (44% versus 42.5%, respectively, p = 0.76). Thus,
option A is incorrect. However, and somewhat paradoxically, in the less severe septic
shock group, vasopressin was associated with a lower mortality rate than norepinephrine
(26.5% versus 35.7%, p = 0.05). The study’s authors consider this finding, though
interesting, to be a subgroup analysis subject to all the statistical shortcomings of
subgroups. This finding was judged to be hypothesis-generating, and future clinical trials
should evaluate its validity.
One of the major side effects of higher doses of vasopressin (usually in the 0.1–0.4 U/min
range) was an increased incidence of acute ischemic heart disease, including myocardial
infarction and death. Presumably, these adverse events resulted from vasopressin-induced
coronary vasoconstriction. The low-dose regimen of 0.01–0.03 U/min was developed to
avoid these side effects, and in fact, VASST had no increase in episodes of ischemic
heart disease associated with vasopressin use. Thus, option B is incorrect. In fact, overall
adverse events were the same in the vasopressin and norepinephrine groups.

Vasopressin is a powerful vasoconstrictor, and in VASST as well as multiple previous
smaller vasopressin studies, vasopressin administration has resulted in a large decrease in
norepinephrine dose when using a target mean BP of 65 to 75 mm Hg. Thus, option D is

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