NUR 2755 MDC4 Final Exam Study Guide: Key
Topics and Practice | with Correct Answers | Graded
A+ | New Version | Rasmussen University
1. A patient with septic shock remains hypotensive despite fluid resuscitation and norepinephrine
infusion. Which hemodynamic profile would most support the addition of vasopressin as a
second-line vasopressor?
A. High cardiac output, low systemic vascular resistance (SVR), low central venous pressure (CVP)
B. Low cardiac output, high SVR, high CVP
C. High cardiac output, high SVR, low CVP
D. Low cardiac output, low SVR, low CVP
Answer: A
Rationale: Vasopressin is indicated in distributive shock (e.g., septic) with high cardiac output and low
SVR, as it increases SVR via V1 receptors. Options B and D reflect cardiogenic or hypovolemic shock,
where vasopressin is not first-line. Option C (high SVR) suggests vasoconstriction already present,
making additional vasopressin less beneficial.
2. A patient with acute respiratory distress syndrome (ARDS) is on volume-controlled ventilation
with plateau pressure of 32 cm H2O and PaO2/FiO2 ratio of 150. Which intervention should the
nurse question?
A. Increasing positive end-expiratory pressure (PEEP) to recruit alveoli
B. Administering a neuromuscular blocking agent to improve oxygenation
C. Increasing tidal volume to 8 mL/kg ideal body weight to improve minute ventilation
D. Trialing prone positioning to enhance ventilation-perfusion matching
Answer: C
Rationale: In ARDS, lung-protective ventilation uses low tidal volumes (4-6 mL/kg) to prevent
volutrauma. Increasing tidal volume to 8 mL/kg would worsen lung injury. Options A, B, and D are
evidence-based strategies to improve oxygenation and reduce ventilator-induced lung injury.
3. A nurse is caring for a patient with acute liver failure and hepatic encephalopathy. Which
assessment finding would be most indicative of worsening cerebral edema?
A. Progressive increase in serum ammonia levels
B. Change from asterixis to decerebrate posturing
C. Decrease in mean arterial pressure (MAP) by 10 mm Hg
D. Increase in urine output to 200 mL/hour
Answer: B
Rationale: Worsening cerebral edema leads to brainstem herniation, manifesting as abnormal posturing
(decerebrate/decorticate). Asterixis is an early sign of encephalopathy but not specific to edema. Serum
ammonia correlates poorly with cerebral edema. Hypotension and polyuria are not direct indicators of
Page 1
,increasing intracranial pressure.
4. A patient with chronic kidney disease (stage 4) is prescribed sevelamer carbonate. The nurse
understands that this medication's primary mechanism of action is to:
A. Bind dietary phosphate in the gastrointestinal tract, reducing absorption
B. Increase renal excretion of phosphate by inhibiting tubular reabsorption
C. Chelate calcium and prevent vascular calcification
D. Alkalinize the urine to prevent phosphate stone formation
Answer: A
Rationale: Sevelamer carbonate is a phosphate binder that works in the GI tract by binding phosphate
from food, preventing its absorption. It does not affect renal excretion (B), chelate calcium (C), or
alkalinize urine (D). It is used in CKD to manage hyperphosphatemia without adding calcium load.
5. A patient with a history of heart failure with reduced ejection fraction (HFrEF) is admitted with
acute decompensation. Which combination of medications would the nurse anticipate being MOST
beneficial for reducing mortality in the long term?
A. Furosemide, metoprolol, and digoxin
B. Lisinopril, carvedilol, and spironolactone
C. Hydralazine, isosorbide dinitrate, and atorvastatin
D. Dobutamine, milrinone, and dopamine
Answer: B
Rationale: Guideline-directed medical therapy for HFrEF includes ACE inhibitors (or ARNIs),
beta-blockers (e.g., carvedilol), and mineralocorticoid receptor antagonists (e.g., spironolactone) to
reduce mortality. Furosemide and digoxin (A) are symptom-relief only. Hydralazine/nitrates (C) are
reserved for African Americans or intolerance. Dobutamine/milrinone (D) are acute inotropic therapies
not for chronic mortality reduction.
6. A nurse is monitoring a patient receiving intravenous heparin for treatment of pulmonary
embolism. The aPTT result is 45 seconds (control 30 seconds). What is the nurse's priority action?
A. Administer protamine sulfate immediately
B. Increase the heparin infusion rate per protocol
C. Decrease the heparin infusion rate per protocol
D. Continue the current infusion rate and recheck aPTT in 6 hours
Answer: B
Rationale: The therapeutic aPTT for heparin is typically 1.5-2.5 times the control, so target is 45-75
seconds. An aPTT of 45 seconds is at the lower end; increasing the rate is appropriate to achieve
therapeutic anticoagulation. Protamine (A) is for reversal of bleeding. Decreasing (C) would be for
supratherapeutic aPTT. Continuing (D) may delay achieving therapeutic levels.
7. A patient with diabetic ketoacidosis (DKA) has an initial serum potassium of 5.2 mEq/L. After
starting insulin and fluids, the nurse anticipates which potassium trend and corresponding
intervention?
Page 2
,A. Potassium will increase further; administer potassium-binding resin
B. Potassium will decrease rapidly; add potassium to IV fluids once level falls below 5.0 mEq/L
C. Potassium will remain stable; no additional monitoring needed
D. Potassium will decrease slowly; begin oral potassium supplementation
Answer: B
Rationale: In DKA, initial hyperkalemia is due to acidosis shifting K+ out of cells. Insulin therapy drives
K+ into cells, causing rapid hypokalemia. Potassium replacement is typically started when K+ is <5.0
mEq/L to prevent life-threatening hypokalemia. Option A is incorrect because K+ decreases. Options C
and D underestimate the risk and timing.
8. A patient with a traumatic brain injury (TBI) has an intracranial pressure (ICP) of 22 mm Hg
and cerebral perfusion pressure (CPP) of 55 mm Hg. Which nursing intervention should be
implemented first?
A. Administer mannitol 0.5 g/kg IV over 30 minutes
B. Elevate the head of bed to 30 degrees and maintain head midline
C. Increase sedation with propofol to decrease metabolic demand
D. Initiate mild hyperventilation to achieve PaCO2 of 30 mm Hg
Answer: B
Rationale: The first intervention for elevated ICP is optimizing venous drainage by elevating HOB and
keeping head midline. This is non-invasive and can quickly reduce ICP. Mannitol (A) is a second-line
osmotic diuretic. Sedation (C) and hyperventilation (D) are later steps; hyperventilation is used
cautiously due to risk of cerebral ischemia.
9. A patient with end-stage renal disease on hemodialysis is admitted with hyperkalemia (K+ 6.8
mEq/L) and ECG changes (peaked T waves). Which sequence of interventions should the nurse
implement first?
A. Administer calcium gluconate IV, then insulin and dextrose IV, then arrange for emergent hemodialysis
B. Administer sodium polystyrene sulfonate (SPS) orally, then albuterol nebulizer, then repeat ECG
C. Start hemodialysis immediately, then administer calcium gluconate if arrhythmias occur
D. Give furosemide IV to promote potassium excretion, then recheck potassium in 2 hours
Answer: A
Rationale: For life-threatening hyperkalemia with ECG changes, first stabilize the myocardium with IV
calcium (prevents arrhythmias), then shift K+ into cells with insulin+dextrose, then definitively remove
K+ via dialysis. SPS (B) is slow and not for emergencies. Dialysis alone (C) without calcium risks
arrhythmias during line placement. Furosemide (D) is ineffective in ESRD.
10. A patient with a history of chronic heart failure presents with worsening dyspnea, jugular
venous distention, and bilateral pitting edema. The nurse reviews the medication list and notes the
patient is on a loop diuretic, an ACE inhibitor, and a beta-blocker. Which laboratory value is most
critical to monitor to prevent a complication of the current therapy?
A. Serum sodium level
B. Serum potassium level
C. Serum magnesium level
Page 3
, D. Serum calcium level
Answer: B
Rationale: Loop diuretics (e.g., furosemide) cause potassium wasting, while ACE inhibitors can cause
potassium retention. The combination increases the risk of hyperkalemia, which can lead to
life-threatening cardiac arrhythmias. Monitoring potassium is essential. Sodium, magnesium, and
calcium are less directly affected by this combination.
11. A patient with acute respiratory distress syndrome (ARDS) is on mechanical ventilation with a
lung-protective strategy. The nurse notes a plateau pressure of 32 cm H2O and a tidal volume of 6
mL/kg predicted body weight. Which intervention should the nurse anticipate to reduce the risk of
ventilator-induced lung injury?
A. Increase positive end-expiratory pressure (PEEP) to 20 cm H2O
B. Decrease tidal volume to 4 mL/kg
C. Administer a neuromuscular blocking agent
D. Switch to pressure-controlled ventilation
Answer: C
Rationale: In ARDS, plateau pressures >30 cm H2O are associated with lung injury. Neuromuscular
blocking agents can reduce patient-ventilator dyssynchrony and decrease oxygen consumption,
potentially lowering plateau pressure. While increasing PEEP may improve oxygenation, it can further
increase plateau pressure. Decreasing tidal volume below 6 mL/kg is not recommended due to risk of
hypercapnia. Switching modes is not directly indicated for reducing plateau pressure.
12. A patient with septic shock requires vasopressor support. The nurse is preparing to administer
norepinephrine. Which hemodynamic parameter indicates that the patient is adequately
volume-resuscitated before initiating the vasopressor?
A. Central venous pressure (CVP) of 4 mm Hg
B. Mean arterial pressure (MAP) of 65 mm Hg
C. Urine output of 0.5 mL/kg/hr
D. Pulmonary artery occlusion pressure (PAOP) of 12 mm Hg
Answer: D
Rationale: A PAOP of 8-12 mm Hg generally indicates adequate preload in septic shock. CVP is less
reliable due to variability. MAP of 65 mm Hg is the target after vasopressor initiation, not a sign of
adequate volume. Urine output is a delayed indicator. Inadequate volume before vasopressors can cause
hypoperfusion.
13. A patient with a traumatic brain injury has an intracranial pressure (ICP) monitor in place.
The nurse observes a sustained ICP of 22 mm Hg for 15 minutes. Which intervention should the
nurse implement first?
A. Administer mannitol 0.5 g/kg IV
B. Elevate the head of bed to 30 degrees
C. Hyperventilate the patient to a PaCO2 of 30 mm Hg
D. Administer propofol sedation
Page 4
Topics and Practice | with Correct Answers | Graded
A+ | New Version | Rasmussen University
1. A patient with septic shock remains hypotensive despite fluid resuscitation and norepinephrine
infusion. Which hemodynamic profile would most support the addition of vasopressin as a
second-line vasopressor?
A. High cardiac output, low systemic vascular resistance (SVR), low central venous pressure (CVP)
B. Low cardiac output, high SVR, high CVP
C. High cardiac output, high SVR, low CVP
D. Low cardiac output, low SVR, low CVP
Answer: A
Rationale: Vasopressin is indicated in distributive shock (e.g., septic) with high cardiac output and low
SVR, as it increases SVR via V1 receptors. Options B and D reflect cardiogenic or hypovolemic shock,
where vasopressin is not first-line. Option C (high SVR) suggests vasoconstriction already present,
making additional vasopressin less beneficial.
2. A patient with acute respiratory distress syndrome (ARDS) is on volume-controlled ventilation
with plateau pressure of 32 cm H2O and PaO2/FiO2 ratio of 150. Which intervention should the
nurse question?
A. Increasing positive end-expiratory pressure (PEEP) to recruit alveoli
B. Administering a neuromuscular blocking agent to improve oxygenation
C. Increasing tidal volume to 8 mL/kg ideal body weight to improve minute ventilation
D. Trialing prone positioning to enhance ventilation-perfusion matching
Answer: C
Rationale: In ARDS, lung-protective ventilation uses low tidal volumes (4-6 mL/kg) to prevent
volutrauma. Increasing tidal volume to 8 mL/kg would worsen lung injury. Options A, B, and D are
evidence-based strategies to improve oxygenation and reduce ventilator-induced lung injury.
3. A nurse is caring for a patient with acute liver failure and hepatic encephalopathy. Which
assessment finding would be most indicative of worsening cerebral edema?
A. Progressive increase in serum ammonia levels
B. Change from asterixis to decerebrate posturing
C. Decrease in mean arterial pressure (MAP) by 10 mm Hg
D. Increase in urine output to 200 mL/hour
Answer: B
Rationale: Worsening cerebral edema leads to brainstem herniation, manifesting as abnormal posturing
(decerebrate/decorticate). Asterixis is an early sign of encephalopathy but not specific to edema. Serum
ammonia correlates poorly with cerebral edema. Hypotension and polyuria are not direct indicators of
Page 1
,increasing intracranial pressure.
4. A patient with chronic kidney disease (stage 4) is prescribed sevelamer carbonate. The nurse
understands that this medication's primary mechanism of action is to:
A. Bind dietary phosphate in the gastrointestinal tract, reducing absorption
B. Increase renal excretion of phosphate by inhibiting tubular reabsorption
C. Chelate calcium and prevent vascular calcification
D. Alkalinize the urine to prevent phosphate stone formation
Answer: A
Rationale: Sevelamer carbonate is a phosphate binder that works in the GI tract by binding phosphate
from food, preventing its absorption. It does not affect renal excretion (B), chelate calcium (C), or
alkalinize urine (D). It is used in CKD to manage hyperphosphatemia without adding calcium load.
5. A patient with a history of heart failure with reduced ejection fraction (HFrEF) is admitted with
acute decompensation. Which combination of medications would the nurse anticipate being MOST
beneficial for reducing mortality in the long term?
A. Furosemide, metoprolol, and digoxin
B. Lisinopril, carvedilol, and spironolactone
C. Hydralazine, isosorbide dinitrate, and atorvastatin
D. Dobutamine, milrinone, and dopamine
Answer: B
Rationale: Guideline-directed medical therapy for HFrEF includes ACE inhibitors (or ARNIs),
beta-blockers (e.g., carvedilol), and mineralocorticoid receptor antagonists (e.g., spironolactone) to
reduce mortality. Furosemide and digoxin (A) are symptom-relief only. Hydralazine/nitrates (C) are
reserved for African Americans or intolerance. Dobutamine/milrinone (D) are acute inotropic therapies
not for chronic mortality reduction.
6. A nurse is monitoring a patient receiving intravenous heparin for treatment of pulmonary
embolism. The aPTT result is 45 seconds (control 30 seconds). What is the nurse's priority action?
A. Administer protamine sulfate immediately
B. Increase the heparin infusion rate per protocol
C. Decrease the heparin infusion rate per protocol
D. Continue the current infusion rate and recheck aPTT in 6 hours
Answer: B
Rationale: The therapeutic aPTT for heparin is typically 1.5-2.5 times the control, so target is 45-75
seconds. An aPTT of 45 seconds is at the lower end; increasing the rate is appropriate to achieve
therapeutic anticoagulation. Protamine (A) is for reversal of bleeding. Decreasing (C) would be for
supratherapeutic aPTT. Continuing (D) may delay achieving therapeutic levels.
7. A patient with diabetic ketoacidosis (DKA) has an initial serum potassium of 5.2 mEq/L. After
starting insulin and fluids, the nurse anticipates which potassium trend and corresponding
intervention?
Page 2
,A. Potassium will increase further; administer potassium-binding resin
B. Potassium will decrease rapidly; add potassium to IV fluids once level falls below 5.0 mEq/L
C. Potassium will remain stable; no additional monitoring needed
D. Potassium will decrease slowly; begin oral potassium supplementation
Answer: B
Rationale: In DKA, initial hyperkalemia is due to acidosis shifting K+ out of cells. Insulin therapy drives
K+ into cells, causing rapid hypokalemia. Potassium replacement is typically started when K+ is <5.0
mEq/L to prevent life-threatening hypokalemia. Option A is incorrect because K+ decreases. Options C
and D underestimate the risk and timing.
8. A patient with a traumatic brain injury (TBI) has an intracranial pressure (ICP) of 22 mm Hg
and cerebral perfusion pressure (CPP) of 55 mm Hg. Which nursing intervention should be
implemented first?
A. Administer mannitol 0.5 g/kg IV over 30 minutes
B. Elevate the head of bed to 30 degrees and maintain head midline
C. Increase sedation with propofol to decrease metabolic demand
D. Initiate mild hyperventilation to achieve PaCO2 of 30 mm Hg
Answer: B
Rationale: The first intervention for elevated ICP is optimizing venous drainage by elevating HOB and
keeping head midline. This is non-invasive and can quickly reduce ICP. Mannitol (A) is a second-line
osmotic diuretic. Sedation (C) and hyperventilation (D) are later steps; hyperventilation is used
cautiously due to risk of cerebral ischemia.
9. A patient with end-stage renal disease on hemodialysis is admitted with hyperkalemia (K+ 6.8
mEq/L) and ECG changes (peaked T waves). Which sequence of interventions should the nurse
implement first?
A. Administer calcium gluconate IV, then insulin and dextrose IV, then arrange for emergent hemodialysis
B. Administer sodium polystyrene sulfonate (SPS) orally, then albuterol nebulizer, then repeat ECG
C. Start hemodialysis immediately, then administer calcium gluconate if arrhythmias occur
D. Give furosemide IV to promote potassium excretion, then recheck potassium in 2 hours
Answer: A
Rationale: For life-threatening hyperkalemia with ECG changes, first stabilize the myocardium with IV
calcium (prevents arrhythmias), then shift K+ into cells with insulin+dextrose, then definitively remove
K+ via dialysis. SPS (B) is slow and not for emergencies. Dialysis alone (C) without calcium risks
arrhythmias during line placement. Furosemide (D) is ineffective in ESRD.
10. A patient with a history of chronic heart failure presents with worsening dyspnea, jugular
venous distention, and bilateral pitting edema. The nurse reviews the medication list and notes the
patient is on a loop diuretic, an ACE inhibitor, and a beta-blocker. Which laboratory value is most
critical to monitor to prevent a complication of the current therapy?
A. Serum sodium level
B. Serum potassium level
C. Serum magnesium level
Page 3
, D. Serum calcium level
Answer: B
Rationale: Loop diuretics (e.g., furosemide) cause potassium wasting, while ACE inhibitors can cause
potassium retention. The combination increases the risk of hyperkalemia, which can lead to
life-threatening cardiac arrhythmias. Monitoring potassium is essential. Sodium, magnesium, and
calcium are less directly affected by this combination.
11. A patient with acute respiratory distress syndrome (ARDS) is on mechanical ventilation with a
lung-protective strategy. The nurse notes a plateau pressure of 32 cm H2O and a tidal volume of 6
mL/kg predicted body weight. Which intervention should the nurse anticipate to reduce the risk of
ventilator-induced lung injury?
A. Increase positive end-expiratory pressure (PEEP) to 20 cm H2O
B. Decrease tidal volume to 4 mL/kg
C. Administer a neuromuscular blocking agent
D. Switch to pressure-controlled ventilation
Answer: C
Rationale: In ARDS, plateau pressures >30 cm H2O are associated with lung injury. Neuromuscular
blocking agents can reduce patient-ventilator dyssynchrony and decrease oxygen consumption,
potentially lowering plateau pressure. While increasing PEEP may improve oxygenation, it can further
increase plateau pressure. Decreasing tidal volume below 6 mL/kg is not recommended due to risk of
hypercapnia. Switching modes is not directly indicated for reducing plateau pressure.
12. A patient with septic shock requires vasopressor support. The nurse is preparing to administer
norepinephrine. Which hemodynamic parameter indicates that the patient is adequately
volume-resuscitated before initiating the vasopressor?
A. Central venous pressure (CVP) of 4 mm Hg
B. Mean arterial pressure (MAP) of 65 mm Hg
C. Urine output of 0.5 mL/kg/hr
D. Pulmonary artery occlusion pressure (PAOP) of 12 mm Hg
Answer: D
Rationale: A PAOP of 8-12 mm Hg generally indicates adequate preload in septic shock. CVP is less
reliable due to variability. MAP of 65 mm Hg is the target after vasopressor initiation, not a sign of
adequate volume. Urine output is a delayed indicator. Inadequate volume before vasopressors can cause
hypoperfusion.
13. A patient with a traumatic brain injury has an intracranial pressure (ICP) monitor in place.
The nurse observes a sustained ICP of 22 mm Hg for 15 minutes. Which intervention should the
nurse implement first?
A. Administer mannitol 0.5 g/kg IV
B. Elevate the head of bed to 30 degrees
C. Hyperventilate the patient to a PaCO2 of 30 mm Hg
D. Administer propofol sedation
Page 4
