,NURS 5334 Advanced Pharmacology: Master
Cardiovascular & Autonomic Drug Therapy Practice
Questions & Detailed Explanations
Subject: NURS 5334 – Advanced Cardiovascular and Autonomic
Pharmacotherapy
Question 1: A patient with heart failure with reduced ejection fraction (HFrEF) is currently stable
on an ACE inhibitor and a beta-blocker. The provider decides to initiate Sacubitril/Valsartan.
Which of the following is a mandatory washout period requirement to mitigate the risk of
angioedema?
A) 12 hours of ACE inhibitor cessation.
B) 24 hours of ACE inhibitor cessation.
C) 36 hours of ACE inhibitor cessation.
D) 48 hours of ACE inhibitor cessation.
Correct Answer: C) 36 hours of ACE inhibitor cessation.
*Explanation: Sacubitril is a neprilysin inhibitor. Neprilysin also degrades bradykinin. If an
ACE inhibitor (which also inhibits bradykinin degradation) is used concurrently with neprilysin
inhibition, the resulting accumulation of bradykinin significantly increases the risk of life-
threatening angioedema. A 36-hour washout period is clinically mandated to allow sufficient
ACE recovery.
Question 2: In a patient experiencing acute decompensated heart failure with significant
cardiogenic shock, which of the following agents acts as a "calcium sensitizer" to increase
cardiac contractility without significantly increasing myocardial oxygen consumption?
A) Dobutamine.
B) Milrinone.
C) Levosimendan.
D) Norepinephrine.
Correct Answer: C) Levosimendan.
*Explanation: Levosimendan stabilizes the cardiac troponin C molecule in its calcium-bound
conformation, increasing contractility (inotropic effect) without increasing intracellular calcium
, concentration. This avoids the high energy expenditure and arrhythmogenic potential associated
with traditional beta-agonists or PDE3 inhibitors.
Question 3: A patient is initiated on Amiodarone for refractory atrial fibrillation. Which baseline
and serial monitoring parameters are most essential due to the unique pharmacodynamic profile
of this agent?
A) CBC, electrolytes, and renal function.
B) Pulmonary function tests (PFTs), TSH, and liver function tests (LFTs).
C) Blood glucose, HbA1c, and lipid panel.
D) Serum drug levels and daily INR.
Correct Answer: B) Pulmonary function tests (PFTs), TSH, and liver function tests (LFTs).
*Explanation: Amiodarone is highly lipid-soluble and contains iodine, leading to systemic
toxicity. It can cause pulmonary fibrosis (requires serial PFTs and CXR), thyroid dysfunction
(hypo- or hyperthyroidism, requires TSH monitoring), and hepatotoxicity (requires LFTs).
Question 4: Which mechanism best explains the rationale for using Ivabradine in patients with
symptomatic HFrEF who have a resting heart rate ≥ 70 bpm despite maximum tolerated beta-
blocker therapy?
A) Inhibition of the inward sodium-potassium current ($I_f$) in the sinoatrial node.
B) Blockade of L-type calcium channels in the myocardial myocytes.
C) Direct stimulation of beta-2 adrenergic receptors.
D) Inhibition of the sarcoplasmic reticulum calcium ATPase pump.
Correct Answer: A) Inhibition of the inward sodium-potassium current ($I_f$) in the
sinoatrial node.
*Explanation: Ivabradine specifically inhibits the $I_f$ current, which is responsible for the
pacemaker activity in the SA node. By slowing the rate of diastolic depolarization, it reduces
heart rate without affecting ventricular contractility or peripheral vascular resistance, unlike
beta-blockers.
Question 5: A patient is on long-term Digoxin therapy and presents with symptoms of toxicity.
Which clinical finding is a classic, though not pathognomonic, ocular manifestation?
A) Myopic shift.
Cardiovascular & Autonomic Drug Therapy Practice
Questions & Detailed Explanations
Subject: NURS 5334 – Advanced Cardiovascular and Autonomic
Pharmacotherapy
Question 1: A patient with heart failure with reduced ejection fraction (HFrEF) is currently stable
on an ACE inhibitor and a beta-blocker. The provider decides to initiate Sacubitril/Valsartan.
Which of the following is a mandatory washout period requirement to mitigate the risk of
angioedema?
A) 12 hours of ACE inhibitor cessation.
B) 24 hours of ACE inhibitor cessation.
C) 36 hours of ACE inhibitor cessation.
D) 48 hours of ACE inhibitor cessation.
Correct Answer: C) 36 hours of ACE inhibitor cessation.
*Explanation: Sacubitril is a neprilysin inhibitor. Neprilysin also degrades bradykinin. If an
ACE inhibitor (which also inhibits bradykinin degradation) is used concurrently with neprilysin
inhibition, the resulting accumulation of bradykinin significantly increases the risk of life-
threatening angioedema. A 36-hour washout period is clinically mandated to allow sufficient
ACE recovery.
Question 2: In a patient experiencing acute decompensated heart failure with significant
cardiogenic shock, which of the following agents acts as a "calcium sensitizer" to increase
cardiac contractility without significantly increasing myocardial oxygen consumption?
A) Dobutamine.
B) Milrinone.
C) Levosimendan.
D) Norepinephrine.
Correct Answer: C) Levosimendan.
*Explanation: Levosimendan stabilizes the cardiac troponin C molecule in its calcium-bound
conformation, increasing contractility (inotropic effect) without increasing intracellular calcium
, concentration. This avoids the high energy expenditure and arrhythmogenic potential associated
with traditional beta-agonists or PDE3 inhibitors.
Question 3: A patient is initiated on Amiodarone for refractory atrial fibrillation. Which baseline
and serial monitoring parameters are most essential due to the unique pharmacodynamic profile
of this agent?
A) CBC, electrolytes, and renal function.
B) Pulmonary function tests (PFTs), TSH, and liver function tests (LFTs).
C) Blood glucose, HbA1c, and lipid panel.
D) Serum drug levels and daily INR.
Correct Answer: B) Pulmonary function tests (PFTs), TSH, and liver function tests (LFTs).
*Explanation: Amiodarone is highly lipid-soluble and contains iodine, leading to systemic
toxicity. It can cause pulmonary fibrosis (requires serial PFTs and CXR), thyroid dysfunction
(hypo- or hyperthyroidism, requires TSH monitoring), and hepatotoxicity (requires LFTs).
Question 4: Which mechanism best explains the rationale for using Ivabradine in patients with
symptomatic HFrEF who have a resting heart rate ≥ 70 bpm despite maximum tolerated beta-
blocker therapy?
A) Inhibition of the inward sodium-potassium current ($I_f$) in the sinoatrial node.
B) Blockade of L-type calcium channels in the myocardial myocytes.
C) Direct stimulation of beta-2 adrenergic receptors.
D) Inhibition of the sarcoplasmic reticulum calcium ATPase pump.
Correct Answer: A) Inhibition of the inward sodium-potassium current ($I_f$) in the
sinoatrial node.
*Explanation: Ivabradine specifically inhibits the $I_f$ current, which is responsible for the
pacemaker activity in the SA node. By slowing the rate of diastolic depolarization, it reduces
heart rate without affecting ventricular contractility or peripheral vascular resistance, unlike
beta-blockers.
Question 5: A patient is on long-term Digoxin therapy and presents with symptoms of toxicity.
Which clinical finding is a classic, though not pathognomonic, ocular manifestation?
A) Myopic shift.
