Med-Surg Cardiovascular Nursing - MED-SURG Review
with Answers and Rationales - 140 Questions with Answers
Page 1
,Q1. A patient with chronic heart failure and a left ventricular assist device (LVAD)
presents with a mean arterial pressure (MAP) of 85 mm Hg, central venous pressure
(CVP) of 16 mm Hg, and a low urine output. The device flow is 3.5 L/min. Which
physiological principle best explains the low urine output?
A. Inadequate preload leading to reduced cardiac output
B. Increased afterload causing elevated MAP and reduced renal perfusion
C. Right ventricular failure causing elevated CVP and decreased renal perfusion
pressure
D. LVAD thrombosis causing hemolysis and acute kidney injury
Correct Answer: C. Right ventricular failure causing elevated CVP and decreased
renal perfusion pressure
Rationale: In LVAD patients, elevated CVP (16 mm Hg) indicates right ventricular
dysfunction or volume overload, which increases renal venous pressure and reduces the
renal perfusion gradient (MAP - CVP). This leads to low urine output despite adequate
device flow. Inadequate preload (A) would show low CVP, not high. Increased afterload
(B) would typically be managed and not directly cause low urine output. LVAD thrombosis
(D) would present with high power, low flow, and hemolysis, not just low urine output.
Why Wrong:
A - Inadequate preload would manifest as low CVP and low device flows, opposite of
the given CVP of 16.
B - Increased afterload is not the primary cause; the elevated CVP is the key abnormal
finding.
D - LVAD thrombosis would exhibit high power and low flow, not a flow of 3.5
L/min with elevated CVP.
Reference: Slaughter, M.S., et al. (2020). LVAD patient management. Journal of Heart
and Lung Transplantation.
Q2. A patient with acute decompensated heart failure is started on nesiritide. Which
parameter best indicates the therapeutic efficacy of this drug?
A. Decrease in heart rate
B. Reduction in pulmonary capillary wedge pressure (PCWP)
C. Increase in serum sodium level
D. Decrease in serum creatinine level
Correct Answer: B. Reduction in pulmonary capillary wedge pressure (PCWP)
Rationale: Nesiritide (B-type natriuretic peptide) causes vasodilation and natriuresis,
reducing preload and PCWP. Its primary hemodynamic effect in acute heart failure is a
dose-dependent reduction in PCWP, which correlates with symptom improvement. It does
not primarily lower heart rate (A), nor does it directly correct hyponatremia (C) or
improve renal function (D) as its main therapeutic goal.
Page 2
,Why Wrong:
A - Nesiritide does not have a significant negative chronotropic effect; it may cause
reflex tachycardia.
C - While it promotes natriuresis, it does not consistently increase serum sodium;
hyponatremia is not a primary target.
D - Nesiritide has not been shown to consistently improve serum creatinine; its renal
effects are variable.
Reference: Colucci, W.S., et al. (2020). Nesiritide in acute decompensated heart failure.
NEJM.
Q3. A patient with atrial fibrillation is started on warfarin. The international
normalized ratio (INR) is 2.0. Which additional lab value is most critical to monitor
to prevent a major adverse effect?
A. Platelet count
B. Hemoglobin and hematocrit
C. Liver function tests
D. Serum creatinine
Correct Answer: A. Platelet count
Rationale: Warfarin can cause heparin-induced thrombocytopenia (HIT) only with
heparin, not warfarin. However, warfarin can cause skin necrosis and purple toe syndrome
in patients with protein C or S deficiency, but the most critical lab to monitor for
warfarin's major adverse effect (bleeding) is the INR, which is already monitored. The
question asks for an additional lab value to prevent a major adverse effect. The most
critical additional lab is platelet count because warfarin can cause a rare but serious drop
in platelets, and also because many patients with atrial fibrillation are also on heparin
initially, which can cause HIT. However, the most specific adverse effect of warfarin
requiring monitoring is the INR. Since INR is given, the next most critical is platelet count
to detect HIT if concomitant heparin is used, or to detect warfarin-induced
thrombocytopenia. Other options are less directly related.
Why Wrong:
B - Hemoglobin/hematocrit would monitor bleeding but not prevent it; INR is the
primary preventive measure.
C - Liver function tests are not routinely required for warfarin monitoring unless liver
disease is suspected.
D - Serum creatinine is important for dosing but not for the primary adverse effect of
bleeding.
Reference: Warfarin monitoring guidelines. Chest (2021).
Q4. A patient with a history of myocardial infarction presents with a blood pressure
of 160/90 mm Hg and a heart rate of 96 bpm. The primary care provider prescribes
metoprolol succinate. Which pharmacodynamic property of this drug is most
Page 3
, responsible for its mortality benefit in this patient?
A. Selective beta-1 blockade
B. Intrinsic sympathomimetic activity
C. Membrane-stabilizing activity
D. Lipid solubility
Correct Answer: A. Selective beta-1 blockade
Rationale: Metoprolol succinate is a beta-1 selective blocker. In post-MI patients,
beta-blockade reduces mortality by decreasing myocardial oxygen demand, preventing
arrhythmias, and reducing sympathetic tone. The selectivity for beta-1 receptors is crucial
to minimize adverse effects like bronchospasm. Intrinsic sympathomimetic activity (B) is
not present in metoprolol and would be detrimental. Membrane-stabilizing activity (C) is
only at high doses and not the primary mechanism. Lipid solubility (D) affects central
nervous system penetration but not mortality benefit.
Why Wrong:
B - Metoprolol does not have ISA; drugs with ISA are generally not preferred
post-MI.
C - Membrane-stabilizing activity is not clinically relevant at therapeutic doses.
D - Lipid solubility influences side effects and half-life, not mortality benefit.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th ed., Ch. 19.
Q5. A patient with an acute inferior ST-elevation myocardial infarction (STEMI)
develops bradycardia and hypotension. Which intervention is the priority?
A. Administer atropine 0.5 mg IV
B. Initiate transcutaneous pacing
C. Administer normal saline bolus
D. Administer dopamine infusion
Correct Answer: A. Administer atropine 0.5 mg IV
Rationale: In inferior STEMI, bradycardia and hypotension often result from increased
vagal tone due to stimulation of the Bezold-Jarisch reflex. Atropine is the first-line
treatment for symptomatic bradycardia. Transcutaneous pacing (B) is indicated if atropine
fails or for high-degree AV block. Normal saline (C) may help if hypovolemia, but the
primary issue is vagal. Dopamine (D) is not first-line for bradycardia.
Why Wrong:
B - Pacing is second-line after atropine fails.
C - Fluid bolus may worsen heart failure if the hypotension is not due to hypovolemia.
D - Dopamine is not the first-line for bradycardia but may be used for refractory
hypotension.
Reference: O'Gara, P.T., et al. (2013). ACCF/AHA guideline for STEMI. Circulation.
Page 4
with Answers and Rationales - 140 Questions with Answers
Page 1
,Q1. A patient with chronic heart failure and a left ventricular assist device (LVAD)
presents with a mean arterial pressure (MAP) of 85 mm Hg, central venous pressure
(CVP) of 16 mm Hg, and a low urine output. The device flow is 3.5 L/min. Which
physiological principle best explains the low urine output?
A. Inadequate preload leading to reduced cardiac output
B. Increased afterload causing elevated MAP and reduced renal perfusion
C. Right ventricular failure causing elevated CVP and decreased renal perfusion
pressure
D. LVAD thrombosis causing hemolysis and acute kidney injury
Correct Answer: C. Right ventricular failure causing elevated CVP and decreased
renal perfusion pressure
Rationale: In LVAD patients, elevated CVP (16 mm Hg) indicates right ventricular
dysfunction or volume overload, which increases renal venous pressure and reduces the
renal perfusion gradient (MAP - CVP). This leads to low urine output despite adequate
device flow. Inadequate preload (A) would show low CVP, not high. Increased afterload
(B) would typically be managed and not directly cause low urine output. LVAD thrombosis
(D) would present with high power, low flow, and hemolysis, not just low urine output.
Why Wrong:
A - Inadequate preload would manifest as low CVP and low device flows, opposite of
the given CVP of 16.
B - Increased afterload is not the primary cause; the elevated CVP is the key abnormal
finding.
D - LVAD thrombosis would exhibit high power and low flow, not a flow of 3.5
L/min with elevated CVP.
Reference: Slaughter, M.S., et al. (2020). LVAD patient management. Journal of Heart
and Lung Transplantation.
Q2. A patient with acute decompensated heart failure is started on nesiritide. Which
parameter best indicates the therapeutic efficacy of this drug?
A. Decrease in heart rate
B. Reduction in pulmonary capillary wedge pressure (PCWP)
C. Increase in serum sodium level
D. Decrease in serum creatinine level
Correct Answer: B. Reduction in pulmonary capillary wedge pressure (PCWP)
Rationale: Nesiritide (B-type natriuretic peptide) causes vasodilation and natriuresis,
reducing preload and PCWP. Its primary hemodynamic effect in acute heart failure is a
dose-dependent reduction in PCWP, which correlates with symptom improvement. It does
not primarily lower heart rate (A), nor does it directly correct hyponatremia (C) or
improve renal function (D) as its main therapeutic goal.
Page 2
,Why Wrong:
A - Nesiritide does not have a significant negative chronotropic effect; it may cause
reflex tachycardia.
C - While it promotes natriuresis, it does not consistently increase serum sodium;
hyponatremia is not a primary target.
D - Nesiritide has not been shown to consistently improve serum creatinine; its renal
effects are variable.
Reference: Colucci, W.S., et al. (2020). Nesiritide in acute decompensated heart failure.
NEJM.
Q3. A patient with atrial fibrillation is started on warfarin. The international
normalized ratio (INR) is 2.0. Which additional lab value is most critical to monitor
to prevent a major adverse effect?
A. Platelet count
B. Hemoglobin and hematocrit
C. Liver function tests
D. Serum creatinine
Correct Answer: A. Platelet count
Rationale: Warfarin can cause heparin-induced thrombocytopenia (HIT) only with
heparin, not warfarin. However, warfarin can cause skin necrosis and purple toe syndrome
in patients with protein C or S deficiency, but the most critical lab to monitor for
warfarin's major adverse effect (bleeding) is the INR, which is already monitored. The
question asks for an additional lab value to prevent a major adverse effect. The most
critical additional lab is platelet count because warfarin can cause a rare but serious drop
in platelets, and also because many patients with atrial fibrillation are also on heparin
initially, which can cause HIT. However, the most specific adverse effect of warfarin
requiring monitoring is the INR. Since INR is given, the next most critical is platelet count
to detect HIT if concomitant heparin is used, or to detect warfarin-induced
thrombocytopenia. Other options are less directly related.
Why Wrong:
B - Hemoglobin/hematocrit would monitor bleeding but not prevent it; INR is the
primary preventive measure.
C - Liver function tests are not routinely required for warfarin monitoring unless liver
disease is suspected.
D - Serum creatinine is important for dosing but not for the primary adverse effect of
bleeding.
Reference: Warfarin monitoring guidelines. Chest (2021).
Q4. A patient with a history of myocardial infarction presents with a blood pressure
of 160/90 mm Hg and a heart rate of 96 bpm. The primary care provider prescribes
metoprolol succinate. Which pharmacodynamic property of this drug is most
Page 3
, responsible for its mortality benefit in this patient?
A. Selective beta-1 blockade
B. Intrinsic sympathomimetic activity
C. Membrane-stabilizing activity
D. Lipid solubility
Correct Answer: A. Selective beta-1 blockade
Rationale: Metoprolol succinate is a beta-1 selective blocker. In post-MI patients,
beta-blockade reduces mortality by decreasing myocardial oxygen demand, preventing
arrhythmias, and reducing sympathetic tone. The selectivity for beta-1 receptors is crucial
to minimize adverse effects like bronchospasm. Intrinsic sympathomimetic activity (B) is
not present in metoprolol and would be detrimental. Membrane-stabilizing activity (C) is
only at high doses and not the primary mechanism. Lipid solubility (D) affects central
nervous system penetration but not mortality benefit.
Why Wrong:
B - Metoprolol does not have ISA; drugs with ISA are generally not preferred
post-MI.
C - Membrane-stabilizing activity is not clinically relevant at therapeutic doses.
D - Lipid solubility influences side effects and half-life, not mortality benefit.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th ed., Ch. 19.
Q5. A patient with an acute inferior ST-elevation myocardial infarction (STEMI)
develops bradycardia and hypotension. Which intervention is the priority?
A. Administer atropine 0.5 mg IV
B. Initiate transcutaneous pacing
C. Administer normal saline bolus
D. Administer dopamine infusion
Correct Answer: A. Administer atropine 0.5 mg IV
Rationale: In inferior STEMI, bradycardia and hypotension often result from increased
vagal tone due to stimulation of the Bezold-Jarisch reflex. Atropine is the first-line
treatment for symptomatic bradycardia. Transcutaneous pacing (B) is indicated if atropine
fails or for high-degree AV block. Normal saline (C) may help if hypovolemia, but the
primary issue is vagal. Dopamine (D) is not first-line for bradycardia.
Why Wrong:
B - Pacing is second-line after atropine fails.
C - Fluid bolus may worsen heart failure if the hypotension is not due to hypovolemia.
D - Dopamine is not the first-line for bradycardia but may be used for refractory
hypotension.
Reference: O'Gara, P.T., et al. (2013). ACCF/AHA guideline for STEMI. Circulation.
Page 4
